Jim Humble

Aerospace engineer Jim Humble’s third career started accidentally while on a gold prospecting trip in the jungle of Venezuela. There, using stabilized oxygen, he improvised an effective remedy for his colleagues who were stricken with malaria. As curious as he had always been in his life, he returned to his native US and wondered why the cure had worked so well.

The answers to his own questions led him to the development of a more powerful form of oxygen therapy, chlorine dioxide, which he called Master Mineral Solution. With a mission to help the human race whatever he did, Jim made it widely available in the form of sodium chlorite which the user ‘activated’ by adding citric acid,lemon juice or vinegar – and medical teams conducted 100,000 research trials in Africa where it was found that MMS 1 would frequently relieve the symptoms of malaria in as little as four hours.

http://jimhumble.biz/

The Science Behind The Treatment On The Mechanisms Of Toxicity Of Chlorine Oxides Against Malarial Parasites – An Overview By Thomas Lee Hesselink, MD. Susan Busse, MD., John Peterson Copyright September 6, 2007

The purpose of this article is to propose research. Nothing in this article is intended as medical advice. No claims, promises or guarantees are made.

ABSTRACT

Sodium chlorite (NaClO2) can be acidified as a convenient method to produce chlorine dioxide (ClO2) which is a strong oxidant and a potent disinfectant. A protocol has been developed whereby a solution of these compounds can be taken orally. This procedure rapidly eliminates malaria and other infectious agents in only one dose.

Chlorine dioxide (ClO2) is highly reactive with thiols, polyamines, purines, certain amino acids and iron, all of which are necessary for the growth and survival of pathogenic microbes. Properly dosed this new treatment is tolerable orally with only transient side effects. More research to better document efficacy in malaria and in other infections is urgently called for.

DISCOVERY

A modern gold prospecting geologist,needed to travel to malaria infested areas numerous times. He or his coworkers would on occasion contract malaria. At times,access to modern medical treatment was absolutely unavailable. Under such dire circumstances it was found that a solution useful to sanitize drinking water was also effective to treat malaria if diluted differently and taken orally. [1a]

Despite no formal medical training the prospector had the innate wisdom to experiment with various dosage and administration techniques. Out of such necessity was invented an easy to use treatment for malaria which was found rapidly effective in almost all cases.

MATERIALS AND METHODS

The procedure as used is as follows: A 28% stock solution of 80% (technical grade) sodium chlorite (NaClO2) is prepared. The remaining 20% is a mixture of the usual excipients necessary in the manufacture and stabilization of sodium chlorite powder or flake. Such are mostly sodium chloride (NaCl) ~19%, sodium hydroxide (NaOH) <1%, and sodium chlorate (NaClO3) <1%. The actual sodium chlorite present is therefore 22.4%. Using a medium caliber dropper (25 drops per cc), the usual administered dose per treatment is 6 to 15 drops. In terms of milligrams of sodium chlorite, this calculates out to 9mg per drop or 54mg to 135mg per treatment. Effectiveness is enhanced, if prior to administration the selected drops are premixed with 2.5 to 5 cc of table vinegar or lime juice or 5-10% citric acid and allowed to react for 3 minutes. The resultant solution is always mixed into a glass of water or apple juice and taken orally. The carboxylic acids neutralize the sodium hydroxide and at the same time convert a small portion of the chlorite (ClO2-) to its conjugate acid known as chlorous acid (HClO2). Under such conditions the chlorous acid will oxidize other chlorite anions and gradually produce chlorine dioxide (ClO2). Chlorine dioxide appears in solution as a yellow tint which smells exactly like elemental chlorine (Cl2). The above described procedure can be repeated a few hours later if necessary. Considerably lower dosing should be applied in children or in emaciated individuals scaled down according to size or weight. The solution can be taken without food to enhance effectiveness but this often causes nausea. Drinking extra water usually relieves this. Nausea is less likely to occur if food is present in the stomach (preferably starchy food not protein) about one hour after a meal. Other side effects reported are transient vomiting, diarrhea, headache, dizziness, lethargy or malaise. Significant amounts of vitamin C (ascorbic acid) must not be present at any point in the mixtures or else this will quench the chlorine dioxide (ClO2) and render it ineffective. For the same reason antioxidant supplements should probably not be taken on the day of treatment.

EXPLORING BENEFITS

We first learned of the acidified sodium chlorite treatment discovery in the fall of 2006. That sodium chlorite or chlorine dioxide could kill parasites in vivo seemed immediately reasonable to us at the onset. It is well known that many disease causing organisms are sensitive to oxidants. Various compounds classifiable as oxides of chlorine such as sodium hypochlorite and chlorine dioxide are already widely used as disinfectants. What is novel and exciting here is that the treatment technique seems: 1) easy to use, 2) rapidly acting, 3) successful, 4) apparently lacking in toxicity, and 5) affordable. If this treatment continues to prove effective, it could be used to help rid the world of one of the most devasting of all known plagues. [3a,3b,3c,3d,3e] Millions of people suffer from malaria year round. One to three million die from malaria every year; most of these are children. This motivated us to learn all we could about the chemistry of the oxides of chlorine. [4a-4hh] We wanted to understand their probable mechanisms of toxicity towards the causative agents of malaria (Plasmodium species), therefore we checked available literature pertaining to issues of safety or risk in human use.

OXIDANTS AS PHYSIOLOGIC AGENTS

Oxidants are atoms or molecules which take up electrons. Reductants are atoms or molecules which donate electrons to oxidants. Dr.Hesselink was already very familiar with most of the medicinally useful oxidants. He has taught at numerous seminars on their use and explained their mechanisms of action on the biochemical level. Examples are: hydrogen peroxide, zinc peroxide, various quinones, various glyoxals, ozone, ultraviolet light, hyperbaric oxygen, benzoyl peroxide, anodes, artemisinin, methylene blue, allicin, iodine and permanganate. Some work has been done using dilute solutions of sodium chlorite internally to treat fungal infections, chronic fatigue, and cancer; however, little has been published in that regard. [5a-5h] Low dose oxidant exposure to living red blood cells induces a change in oxyhemoglobin (Hb-O2) activity so that more oxygen (O2) is released to tissues throughout the body. [6a-6d] Hyperbaric oxygenation (oxygen under pressure) is: 1) a powerful detoxifier against carbon monoxide; 2) a powerful support for natural healing in burns, crush injuries, and ischemic strokes; and 3) an effective aid to treat most bacterial infections. [7a-7d] Taken internally, intermittently and in low doses many oxidants have been found to be powerful immune stimulants. Sodium chlorite acidified with lactic acid as in the product “WF10″ has similarly been shown to modulate immune activation. Exposure of live blood to ultraviolet light also has immune enhancing effects. These treatments work through a natural physiologic trigger mechanism, which induces peripheral white blood cells to express and to release cytokines. These cytokines serve as a control system to down-regulate allergic reactions and as an alarm system to increase cellular attack against pathogens. [8a-8v] Activated cells of the immune system naturally produce strong oxidants as part of the inflammatory process at sites of infection or cancer to rid the body of these diseases. Examples are: superoxide (*OO-), hydrogen peroxide (H2O2), hydroxyl radical (HO*), singlet oxygen (O=O) and ozone (O3). [9a-9v] Another is peroxynitrate (-OONO) the coupled product of superoxide (*OO-) and nitric oxide (*NO) radicals. [10a-10h] Yet another is hypochlorous acid (HOCl) the conjugate acid of sodium hypochlorite (NaClO). [11a,11b,11c] The immune system uses these oxidants to attack various parasites. [12a,12b,12c]

OXIDES OF CHLORINE AS DISINFECTANTS

All bacteria have been shown to be incabable of growing in any medium in which the oxidants (electron grabbers) out- number the reductants (electron donors). [13a] Therefore, oxidants are at least bacteriostatic and at most are bacteriocidal. [13b] Many oxidants have been proven useful as antibacterial disinfectants. [13c,13d] Hypochlorites (ClO-) are commonly used as bleaching agents, as swimming pool sanitizers, and as disinfectants. At low concentrations chlorine dioxide (ClO2) has been shown to kill many types of bacteria [14a-14j], viruses [15a-15L] and protozoa [16a-16f]. Ozone (O3) or chlorine dioxide (ClO2) are often used to disinfect public water supplies or to sanitize and deodorize waste water. [17a-17L] Sodium chlorite (NaClO2) or chlorine dioxide (ClO2) solutions are used in certain mouth washes to clear mouth odors and oral bacteria. [18a-18i] Chlorine dioxide sanitizes food preparation facilities. [19a] Acidified sodium chlorite is FDA approved as a spray in the meat packing industry to sanitized meat. [20a-20g] This can also be used to sanitize vegetables and other foods. [21a,21b] Farmers use this to cleanse the udders of cows to prevent mastitis, [22a,22b,22c] or to rid eggs of pathogenic bacteria. Chlorine dioxide can be used to disinfect endoscopes. [23a] Oxidants such as iodine, various peroxides, permanganate and chlorine dioxide can be applied topically to the skin to treat infections caused by bacteria or fungi. [24a-24d]

MALARIA IS OXIDANT SENSITIVE

Dr. Hesselink, scientific researcher spent hundreds of hours searching biochemical literature and medical literature pertaining to the biochemistry of Plasmodia. Four species are commonly pathogenic in humans namely: Plasmodium vivax, Plasmodium falciparum, Plasmodium ovale and Plasmodium malariae. What he found was an abundance of confirmation that, just like bacteria, Plasmodia are indeed quite sensitive to oxidants. [25a-25m]. Examples of oxidants toxic to Plasmodia include: artemisinin, artemether [26a-26m], t-butyl hydroperoxide [27a], xanthone [28a], various quinones [29a-29m] (e.g. atovaquone, lapachol, beta-lapachone, menadione) and methylene blue [30a-30i].

TARGETING THIOLS

Like bacteria, fungi and tumor cells, the ability of Plasmodia to live and grow depends heavily on an internal abundance of reductants. This is especially true regarding thiol compounds also known as sulfhydryl compounds (RSH). [31a,31b] Thiols as a class behave as reductants (electron donors). As such they are especially sensitive to oxidants (electron grabbers). Thiols (RSH) such as glutathione [32a-32L] and other sulfur compounds [33a,33b,33c] are reactive with sodium chlorite (NaClO2) and with chlorine dioxide (ClO2). These are the very agents present in the acidified sodium chlorite solution. The products of oxidation of thiols (RSH) using various oxides of chlorine are: disulfides (RSSR), disulfide monoxides (RSSOR), sulfenic acids (RSOH), sulfinic acids (RSO2H), and sulfonic acids (RSO3H). None of these can support the life processes of the parasite. Upon sufficient removal of the parasite’s life sustaining thiols by oxidation, the parasite rapidly dies. [34a-34e] A list of thiols (RSH) upon which survival of Plasmodium species heavily depend includes: lipoic acid and dihydrolipoic acid [35a-35h], coenzyme A and acyl carrier protein [36a-36f], glutathione [37a-37m], glutathione reductase [38a-38e], glutathione-S-transferase [39a-39g], peroxiredoxin [40a-40L], thioredoxin [41a-41g], glutaredoxin [42a,42b,42c], plasmoredoxin [43a], thioredoxin reductase [44a-44g], falcipain [45a-45i], and ornithine decarboxylase [46a-46e].

HEME IS AN OXIDANT SENSITIZER

Of particular relevance to treating malaria is the fact that Plasmodial trophozoites living inside red blood cells must digest hemoglobin as their preferred protein source. [47a,47b] They accomplish this by ingesting hemoglobin into an organelle known as the “acid food vacuole”. [47c-47h] Incidently, the high concentration of acid in this organelle could serve as an additional site of conversion of chlorite (ClO2-) to the more active chlorine dioxide (ClO2) right inside the parasite. Furthermore, Plasmodia consume 50 to 100 times more glucose than noninfected red blood cells most of which is metabolized to lactic acid a known activator of chlorite. [48a-48b] Next falcipain (a hemoglobin digesting enzyme) hydrolyzes hemoglobin protein to release its nutritional amino acids. [49a-49e] A necessary byproduct of this digestion is the release of 4 heme molecules from each hemoglobin molecule digested. Free heme (also known as ferriprotoporphyrin IX) is redox active and can react with ambient oxygen (O2), an abundance of which is always present in red blood cells. This produces superoxide radical (*OO-), hydrogen peroxide (H2O2) and other reactive oxidant toxic species (ROTS). [50a-50bb]. These can rapidly poison the parasite internally. To protect themselves against this dangerous side-effect of eating blood protein, Plasmodia must maintain a high reductant capacity (an abundance of reduced thiols and NADPH) to quench these ROTS. This is their main mechanism of antioxidant defense. [51a-51n] Plasmodia must also rapidly and continuously eliminate heme , which is accomplished by two methods. 1) heme is polymerized producing hemozoin. [52a-52k] 2) heme is metabolized in a detoxification process that requires reduced glutathione (GSH). [53a,53b] Therefore any method (especially exposure to oxidants) which limits the availability of reduced glutathione (GSH) will cause a toxic build up of heme and of ROTS inside the parasite cells. Sodium chlorite and chlorine dioxide (the exact agents present in the acidified sodium chlorite treatment) readily oxidize glutathione. [54a,54b] Therefore, a rapid killing of Plasmodia upon taking acidified sodium chlorite orally should be expected.

OVERCOMING ANTIBIOTIC RESISTANCE WITH OXIDATION

Now the issue of resistance of Plasmodium species to commonly used antiprotozoal antibiotics must be addressed. Quinine, chloroquine, mefloquine, quinacrine, amodiaquine, primaquine and other quinoline-like antibiotics all work by blocking the heme detoxifying system inside the trophozoites. [55a-55gg] Many Plasmodial strains against which quinolines have repeatedly been used have found ways to adapt to these drugs and to acquire resistance. Research into the mechanisms of resistance has found that often resistance is accomplished by a meere upregulation of glutathione production and utilization. [56a-56j] Consequently oxidizing or otherwise depleting glutathione inside the parasite usually restores sensitivity to the quinoline antibiotics. [57a-57f] Therefore, protocols combining the use of oxidants with quinolines are under developement and already showing signs of success. [57g] In this context let us consider that no amount of intraplasmodial glutathione (GSH) could ever resist exposure to a suffient dose of chlorine dioxide (ClO2). Note that each molecule of ClO2 can disable 1 to 5 molecules of glutathione depending on the reaction mechanism. 2(GSH) + 2(ClO2) -> 1(GSSG) + 2(H+) + 2(ClO2-) or 10(GSH) + 2(ClO2) -> 5(GSSG) + 2(H+) + 2(Cl-) + 4(H2O)

SOME INCOMPATIBILITIES

Acidified sodium chlorite could provide a powerful new opportunity to improve or to restore sensitivity to quinolines by virtue of its oxidative power. However, quinolines contain secondary or tertiary amino groups which react with chlorine dioxide in such a way that both could destroy each other. Some possible strategies to resolve this incompatibility are suggested below.

Acidified sodium chlorite could be used as explained above only as a solo therapy.

Quinoline administration could be withheld until after the acidified sodium chorite has completed its action.

Patients already preloaded with a quinoline could stop this, wait a suitable period of time for this to wash out, then administer the acidified sodium chlorite.

The quinoline could remain in use and while the less active sodium chlorite is administered without acid. This should retain plenty of oxidant effectiveness without destroying any quinoline or wasting too much oxidant.

Switch from a quinoline to an endoperoxide (such as artemisinin) or to a quinone (such as atovaquone) before using acidified sodium chlorite, as these may be less sensitive toward destruction by chlorine dioxide.

Similar problems apply to methylene blue and many other drugs if they have an unoxidized sulfur atom, a phenol group, a secondary amine or a tertiary amine. Such are also very reactive with the chlorine dioxide component. [58a]

REDUCTANT RECOVERY SYSTEMS

Living things possess a recovery system to rescue oxidized sulfur compounds. It operates through donation of hydrogen atoms to these compounds and thereby restores their original condition as thiols. [59a,59b] 2 [H] + (GSSG) -> 2(GSH) This system is known as the hexose monophophate shunt.[59c,59d] A key player in this system is the enzyme glucose-6-phosphate-dehydrogenase (G6PDH). Patients with a genetic defect of G6PDH, known as glucose-6-phosphate-dehydrogenase deficiency disease, are especially sensitive to oxidants and to prooxidant drugs. However, this genetic disease has a benefit in that such individuals are naturally resistant to malaria. They can still catch malaria, but it is much less severe in them, since they permanently lack the enzyme necessary to assist the parasite in reactivating glutathione and other oxidized thiols. [60a-60h] Chlorine dioxide (ClO2) has been shown to oxidize and denature G6PDH by reaction with tyrosine and tryptophan residues inside the enzyme. [61a] Furthermore, G6PDH is sensitive to inhibition by sodium chlorate (NaClO3), another member of the chlorine oxide family of compounds. [61b,61c,61d] Sodium chlorate (NaClO3) is a trace ingredient present in the acicified sodium chlorite antimalarial solution. Some sodium chlorate (NaClO3) should also be produced in vivo by a slow reaction of chlorine dioxide (ClO2) with water under alkaline conditions [61e]. 2(ClO2) + 2(OH-) -> (ClO2-) + (ClO3-) + H2O

The Plasmodia may attempt to restore any thiols (RSH) lost to oxidation. However, this becomes more difficult as G6PDH is inhibited by chlorine dioxide (ClO2) or by chlorate (ClO3-).

TARGETING IRON

While most available literature refers to redox imbalances causing depletion of necessary thiols, other mechanisms of toxicity of the oxides of chlorine against Plasmodia should also be considered. Oxides of chlorine are generally rapidly reactive with ferrous iron (Fe++) converting it to ferric (Fe+++). [62a-62d] This explains why in cases of overdosed exposures to oxides of chlorine such as sodium chlorite (NaClO2) there was a notable rise in methemoglobin levels. [63a,63b] Methemoglobin is a metabolically inactive form of hemoglobin in which its ferrous iron (Fe++) cofactor has been oxidized to ferric (Fe+++). In living things including parasites iron is a necessary cofactor for many enzymes. [64a-64f] Thus it is reasonable to expect that any damage to Plasmodia caused by oxides of chlorine is compounded by conversion of ferrous (Fe++) cofactors to ferric (Fe+++) or other alterations of iron compounds. [65a-65g] Superoxide dismutase (SOD) inside Plasmodial cells utilizes iron in its active center. [66a-66m] Chlorine dioxide also oxidizes manganese. [67a]

TARGETING POLYAMINES

Other metabolites necessary for survival and growth in tumors, bacteria and parasites are the polyamines. [68a-68d] Plasmodia quit growing and die, when polyamines are lacking [69a-69k], or when their functions are blocked [70a-70L]. Polyamines are also sensitive to oxidation and can be eliminated by strong oxidants. When oxidized, polyamines are converted to aldehydes, which are deadly to parasites and to tumors. [71a-71e] Chlorine dioxide (ClO2) is known to be especially reactive against secondary amines. [72a] This includes spermine and spermidine the two main biologically important polyamines. Thus any procedure which is successful to oxidize both thiols and polyamines does quadruple damage to the pathogen: oxidation of the thiol ornithine decarboxylase inhibits polyamine synthesis;oxidation of the thiol S-adenosyl-L-methionine decarboxylase also inhibits polyamine synthesis; (see references below and in “Targeting Thiols” above)oxidation of the secondary amines spermidine and spermine depletes polyamine supplies;the products of polyamine oxidation are toxic aldehydes.

TARGETING PURINES

Purines are essential to many life processes. These molecules have a double ring structure. The rings are heterocyclic being composed of both carbon and nitrogen. Their nitrogen atoms are vulnerable to reaction with chlorine dioxide. [73a] Examples of important biologic purines are xanthine, hypoxanthine, inosine, guanine and adenine. Guanine and adenine are essential components of DNA and RNA necessary for all genetic functions and for all protein syntheses. Adenine is an essential component of the cofactors NADH, NADPH, FAD and ATP, necessary for many metabolic functions including oxidation-reduction and energy metabolism. Any purines lost by chlorine dioxide exposure can be readily replaced by host cells. [74a] Plasmodia and other apicomplexae are uniquely vulnerable to purine deficiency as they lack the enzymes necessary to produce purines for themselves [75a,75b,75c]. Instead these must be scavenged from host cells and imported across the plasma membranes of the parasite cells. [76a-76i] Drugs are under development to inhibit purine utilization by Plasmodia and are already showing signs of success. [77a-77g] Temporarily destroying some of the purines in the blood as should occur upon brief exposure to chlorine dioxide in vivo is probably an additional stress that Plasmodia cannot tolerate.

TARGETING PROTEINS

Chlorine dioxide (ClO2) is highly reactive with thiols, phenols, secondary amines and tertiary amines. Therefore, proteins composed of amino acids which present these reactive groups are vulnerable to oxidation by this agent. Proteins which present residue(s) of the amino acid L-cysteine are discussed above under TARGETING THIOLS. L-tyrosine presents a phenol group and is therefore similarly vulnerable. L-tryptophan and L-histidine present secondary amino groups which are also especially reactive with chlorine dioxide. [78a-78d]

SAFETY ISSUES

A remaining concern is safety. So far, at least anecdotally, the dosages of chlorine oxides as administered orally per the acidified sodium chlorite protocol have produced no definite toxicity. Some have taken this as often as 1 to 3 times weekly and on the surface seem to suffer no ill effects. To be certain if this is safe more research is warranted for such long term or repeated use. The concern is that too much or too frequent administration of oxidants could excessively deplete the body’s reductants and promote oxidative stress. One useful way to monitor this may be to periodically check methemoglobin levels in frequent users. Sodium chlorite, as found in municipal water supplies after disinfection by chorine dioxide, has been studied and proven safe. [79a-79i] Animal studies using much higher oral or topical doses have proven relatively safe. [80a-80p] In a suicide attempt 10g of sodium chlorite taken orally caused nearly fatal kidney failure and refractory methemoglobinemia. [81a] Inhalation or aerosol exposure to chlorine dioxide gas is highly irritating and generally not recommended. [82a-82g] Special precautions must be employed in cases of glucose-6-phosphate-dehydrogenase deficiency disease, as these patients are especially sensitive to oxidants of all kinds. [83a-83g] Nevertheless, oral acidified sodium chlorite solutions might even be found safe [84a,84b] and effective in them, but probably will need to be administered at lower doses.

MORE RESEARCH

It is hoped that this overview will spark a flurry of interest, and stimulate more research into the use of acidified sodium chlorite in the treatment of malaria. The above appreciated observations need to be proven more rigorously and published [85a]. The biochemistry most likely involved suggests that other members of the phylum Apicomplexa should also be sensitive to this treatment. [86a] This phylum includes: Plasmodium, Babesia, Toxoplasma [87a], Cryptosporidium [88a], Eimeria, Theileria, Sarcocystis, Cyclospora, Isospora and Neospora. These pathogens are responsible for widespread diseases in humans, pets and cattle. Other thiol dependent parasites should also be susceptible to acidified sodium chlorite. For example Trypanosoma and Leishmania extensively utilize and cannot survive without the cofactor known as trypanothione. Each molecule of trypanothione presents 2 sulfur atoms and 5 secondary amino groups all of which are vulnerable to oxidative destruction from chlorine dioxide (ClO2). [89a-89p]

Chlorine dioxide has been proven to be cidal to almost all known infectious agents in vitro using remarkably low concentrations. This includes parasites, fungi, bacteria and viruses. The experiences noted above imply that this compound is tolerable orally at effective concentrations. [90a,90b] Therefore extensive research is warranted to determine if acidified sodium chlorite is effective in treating other infections. We may be on the verge of discovering the most potent and broad spectrum antimicrobial agent yet known. Special thanks go to all those that are involved in the Malaria Initiative.

*****************************************************************************************************************************

1)ABSTRACT

2)DISCOVERY

3)EXPLORING BENEFITS

4)HEME IS AN OXIDANT SENSITIZER

5)MALARIA IS OXIDANT SENSITIVE

6)MATERIALS AND METHODS

7)MORE RESEARCH

8)OVERCOMING ANTIBIOTIC RESISTANCE WITH OXIDATION

9)OXIDANTS AS PHYSIOLOGIC AGENTS

10)OXIDES OF CHLORINE AS DISINFECTANTS

11)REDUCTANT RECOVERY SYSTEMS

12)SAFETY ISSUES

13)SOME INCOMPATIBILITIES

14)TARGETING IRON

15)TARGETING POLYAMINES

16)TARGETING PROTEINS

17)TARGETING PURINES

18)TARGETING THIOLS

ABSTRACT

On The Mechanisms Of Toxicity Of Chlorine Oxides Against Malarial Parasites – An Overview By Thomas Lee Hesselink, MD. Susan Busse, MD., John Peterson Copyright September 6, 2007

The purpose of this article is to propose research. Nothing in this article is intended as medical advice. No claims, promises or guarantees are made.

1)ABSTRACT

Sodium chlorite (NaClO2) can be acidified as a convenient method to produce chlorine dioxide (ClO2) which is a strong oxidant and a potent disinfectant. A protocol has been developed whereby a solution of these compounds can be taken orally. This procedure rapidly eliminates malaria and other infectious agents in only one dose. Chlorine dioxide (ClO2) is highly reactive with thiols, polyamines, purines, certain amino acids and iron, all of which are necessary for the growth and survival of pathogenic microbes. Properly dosed this new treatment is tolerable orally with only transient side effects. More research to better document efficacy in malaria and in other infections is urgently called for.

2)DISCOVERY

A modern gold prospecting geologist,needed to travel to malaria infested areas numerous times. He or his coworkers would on occasion contract malaria. At times,access to modern medical treatment was absolutely unavailable. Under such dire circumstances it was found that a solution useful to sanitize drinking water was also effective to treat malaria if diluted differently and taken orally. [1a] Despite no formal medical training the prospector had the innate wisdom to experiment with various dosage and administration techniques. Out of such necessity was invented an easy to use treatment for malaria which was found rapidly effective in almost all cases.

3)EXPLORING BENEFITS

We first learned of the acidified sodium chlorite treatment discovery in the fall of 2006. That sodium chlorite or chlorine dioxide could kill parasites in vivo seemed immediately reasonable to us at the onset. It is well known that many disease causing organisms are sensitive to oxidants. Various compounds classifiable as oxides of chlorine such as sodium hypochlorite and chlorine dioxide are already widely used as disinfectants. What is novel and exciting here is that the treatment technique seems:

1) easy to use,

2) rapidly acting,

3) successful,

4) apparently lacking in toxicity, and

5) affordable.

If this treatment continues to prove effective, it could be used to help rid the world of one of the most devasting of all known plagues. [3a-3e]

Millions of people suffer from malaria year round. One to three million die from malaria every year; most of these are children. This motivated us to learn all we could about the chemistry of the oxides of chlorine. [4a-4hh] We wanted to understand their probable mechanisms of toxicity towards the causative agents of malaria (Plasmodium species), therefore we checked available literature pertaining to issues of safety or risk in human use.

4)HEME IS AN OXIDANT SENSITIZER

Of particular relevance to treating malaria is the fact that Plasmodial trophozoites living inside red blood cells must digest hemoglobin as their preferred protein source. [47a,47b] They accomplish this by ingesting hemoglobin into an organelle known as the “acid food vacuole”. [47c-47h] Incidently, the high concentration of acid in this organelle could serve as an additional site of conversion of chlorite (ClO2-) to the more active chlorine dioxide (ClO2) right inside the parasite. Furthermore, Plasmodia consume 50 to 100 times more glucose than noninfected red blood cells most of which is metabolized to lactic acid a known activator of chlorite. [48a-48b]

Next falcipain (a hemoglobin digesting enzyme) hydrolyzes hemoglobin protein to release its nutritional amino acids. [49a-49e] A necessary byproduct of this digestion is the release of 4 heme molecules from each hemoglobin molecule digested. Free heme (also known as ferriprotoporphyrin IX) is redox active and can react with ambient oxygen (O2), an abundance of which is always present in red blood cells. This produces superoxide radical (*OO-), hydrogen peroxide (H2O2) and other reactive oxidant toxic species (ROTS). [50a-50bb]. These can rapidly poison the parasite internally. To protect themselves against this dangerous side-effect of eating blood protein, Plasmodia must maintain a high reductant capacity (an abundance of reduced thiols and NADPH) to quench these ROTS. This is their main mechanism of antioxidant defense. [51a-51n] Plasmodia must also rapidly and continuously eliminate heme , which is accomplished by two methods.

1) heme is polymerized producing hemozoin. [52a-52k]

2) heme is metabolized in a detoxification process that requires reduced glutathione (GSH). [53a,53b]

Therefore any method (especially exposure to oxidants) which limits the availability of reduced glutathione (GSH) will cause a toxic build up of heme and of ROTS inside the parasite cells. Sodium chlorite and chlorine dioxide (the exact agents present in the acidified sodium chlorite treatment) readily oxidize glutathione. [54a,54b] Therefore, a rapid killing of Plasmodia upon taking acidified sodium chlorite orally should be expected.

5)MALARIA IS OXIDANT SENSITIVE

Dr. Hesselink, scientific researcher spent hundreds of hours searching biochemical literature and medical literature pertaining to the biochemistry of Plasmodia. Four species are commonly pathogenic in humans namely: Plasmodium vivax, Plasmodium falciparum, Plasmodium ovale and Plasmodium malariae. What he found was an abundance of confirmation that, just like bacteria, Plasmodia are indeed quite sensitive to oxidants. [25a-25m]. Examples of oxidants toxic to Plasmodia include: artemisinin, artemether [26a-26m], t-butyl hydroperoxide [27a], xanthone [28a], various quinones [29a-29m] (e.g. atovaquone, lapachol, beta-lapachone, menadione) and methylene blue [30a-30i].

6)MATERIALS AND METHODS

The procedure as used is as follows: A 28% stock solution of 80% (technical grade) sodium chlorite (NaClO2) is prepared. The remaining 20% is a mixture of the usual excipients necessary in the manufacture and stabilization of sodium chlorite powder or flake. Such are mostly sodium chloride (NaCl) ~19%, sodium hydroxide (NaOH) <1%, and sodium chlorate (NaClO3) <1%. The actual sodium chlorite present is therefore 22.4%. Using a medium caliber dropper (25 drops per cc), the usual administered dose per treatment is 6 to 15 drops. In terms of milligrams of sodium chlorite, this calculates out to 9mg per drop or 54mg to 135mg per treatment. Effectiveness is enhanced, if prior to administration the selected drops are premixed with 2.5 to 5 cc of table vinegar or lime juice or 5-10% citric acid and allowed to react for 3 minutes. The resultant solution is always mixed into a glass of water or apple juice and taken orally. The carboxylic acids neutralize the sodium hydroxide and at the same time convert a small portion of the chlorite (ClO2-) to its conjugate acid known as chlorous acid (HClO2). Under such conditions the chlorous acid will oxidize other chlorite anions and gradually produce chlorine dioxide (ClO2). Chlorine dioxide appears in solution as a yellow tint which smells exactly like elemental chlorine (Cl2). The above described procedure can be repeated a few hours later if necessary. Considerably lower dosing should be applied in children or in emaciated individuals scaled down according to size or weight. The solution can be taken without food to enhance effectiveness but this often causes nausea. Drinking extra water usually relieves this. Nausea is less likely to occur if food is present in the stomach (preferably starchy food not protein) about one hour after a meal. Other side effects reported are transient vomiting, diarrhea, headache, dizziness, lethargy or malaise. Significant amounts of vitamin C (ascorbic acid) must not be present at any point in the mixtures or else this will quench the chlorine dioxide (ClO2) and render it ineffective. For the same reason antioxidant supplements should probably not be taken on the day of treatment.

7)MORE RESEARCH

It is hoped that this overview will spark a flurry of interest, and stimulate more research into the use of acidified sodium chlorite in the treatment of malaria. The above appreciated observations need to be proven more rigorously and published [85a]. The biochemistry most likely involved suggests that other members of the phylum Apicomplexa should also be sensitive to this treatment. [86a] This phylum includes: Plasmodium, Babesia, Toxoplasma [87a], Cryptosporidium [88a], Eimeria, Theileria, Sarcocystis, Cyclospora, Isospora and Neospora. These pathogens are responsible for widespread diseases in humans, pets and cattle. Other thiol dependent parasites should also be susceptible to acidified sodium chlorite. For example Trypanosoma and Leishmania extensively utilize and cannot survive without the cofactor known as trypanothione. Each molecule of trypanothione presents 2 sulfur atoms and 5 secondary amino groups all of which are vulnerable to oxidative destruction from chlorine dioxide (ClO2). [89a-89p]

Chlorine dioxide has been proven to be cidal to almost all known infectious agents in vitro using remarkably low concentrations. This includes parasites, fungi, bacteria and viruses. The experiences noted above imply that this compound is tolerable orally at effective concentrations. [90a,90b] Therefore extensive research is warranted to determine if acidified sodium chlorite is effective in treating other infections. We may be on the verge of discovering the most potent and broad spectrum antimicrobial agent yet known. Special thanks go to all those that are involved in the Malaria Initiative.

8)OVERCOMING ANTIBIOTIC RESISTANCE WITH OXIDATION

Now the issue of resistance of Plasmodium species to commonly used antiprotozoal antibiotics must be addressed. Quinine, chloroquine, mefloquine, quinacrine, modiaquine, primaquine and other quinoline-like antibiotics all work by blocking the heme detoxifying system inside the trophozoites. [55a-55gg] Many Plasmodial strains against which quinolines have repeatedly been used have found ways to adapt to these drugs and to acquire resistance. Research into the mechanisms of resistance has found that often resistance is accomplished by a meere upregulation of glutathione production and utilization. [56a-56j] Consequently oxidizing or otherwise depleting glutathione inside the parasite usually restores sensitivity to the quinoline antibiotics. [57a-57f] Therefore, protocols combining the use of oxidants with quinolines are under developement and already showing signs of success. [57g] In this context let us consider that no amount of intraplasmodial glutathione (GSH) could ever resist exposure to a suffient dose of chlorine dioxide (ClO2). Note that each molecule of ClO2 can disable 1 to 5 molecules of glutathione depending on the reaction mechanism. 2(GSH) + 2(ClO2) -> 1(GSSG) + 2(H+) + 2(ClO2-) or 10(GSH) + 2(ClO2) -> 5(GSSG) + 2(H+) + 2(Cl-) + 4(H2O)

9)OXIDANTS AS PHYSIOLOGIC AGENTS

Oxidants are atoms or molecules which take up electrons. Reductants are atoms or molecules which donate electrons to oxidants. Dr.Hesselink was already very familiar with most of the medicinally useful oxidants. He has taught at numerous seminars on their use and explained their mechanisms of action on the biochemical level. Examples are: hydrogen peroxide, zinc peroxide, various quinones, various glyoxals, ozone, ultraviolet light, hyperbaric oxygen, benzoyl peroxide, anodes, artemisinin, methylene blue, allicin, iodine and permanganate. Some work has been done using dilute solutions of sodium chlorite internally to treat fungal infections, chronic fatigue, and cancer; however, little has been published in that regard. [5a-5h]

Low dose oxidant exposure to living red blood cells induces a change in oxyhemoglobin (Hb-O2) activity so that more oxygen (O2) is released to tissues throughout the body. [6a-6d] Hyperbaric oxygenation (oxygen under pressure) is:

1) a powerful detoxifier against carbon monoxide;

2) a powerful support for natural healing in burns, crush injuries, and ischemic strokes; and

3) an effective aid to treat most bacterial infections. [7a-7d]

Taken internally, intermittently and in low doses many oxidants have been found to be powerful immune stimulants. Sodium chlorite acidified with lactic acid as in the product “WF10″ has similarly been shown to modulate immune activation. Exposure of live blood to ultraviolet light also has immune enhancing effects. These treatments work through a natural physiologic trigger mechanism, which induces peripheral white blood cells to express and to release cytokines. These cytokines serve as a control system to down-regulate allergic reactions and as an alarm system to increase cellular attack against pathogens. [8a-8v]

Activated cells of the immune system naturally produce strong oxidants as part of the inflammatory process at sites of infection or cancer to rid the body of these diseases. Examples are: superoxide (*OO-), hydrogen peroxide (H2O2), hydroxyl radical (HO*), singlet oxygen (O=O) and ozone (O3). [9a-9v] Another is peroxynitrate (-OONO) the coupled product of superoxide (*OO-) and nitric oxide (*NO) radicals. [10a-10h] Yet another is hypochlorous acid (HOCl) the conjugate acid of sodium hypochlorite (NaClO). [11a,11b,11c] The immune system uses these oxidants to attack various parasites. [12a,12b,12c]

10)OXIDES OF CHLORINE AS DISINFECTANTS

All bacteria have been shown to be incabable of growing in any medium in which the oxidants (electron grabbers) out-number the reductants (electron donors). [13a] Therefore, oxidants are at least bacteriostatic and at most are bacteriocidal. [13b] Many oxidants have been proven useful as antibacterial disinfectants. [13c,13d] Hypochlorites (ClO-) are commonly used as bleaching agents, as swimming pool sanitizers, and as disinfectants. At low concentrations chlorine dioxide (ClO2) has been shown to kill many types of bacteria [14a-14j], viruses [15a-15L] and protozoa [16a-16f]. Ozone (O3) or chlorine dioxide (ClO2) are often used to disinfect public water supplies or to sanitize and deodorize waste water. [17a-17L] Sodium chlorite (NaClO2) or chlorine dioxide (ClO2) solutions are used in certain mouth washes to clear mouth odors and oral bacteria. [18a-18i] Chlorine dioxide sanitizes food preparation facilities. [19a] Acidified sodium chlorite is FDA approved as a spray in the meat packing industry to sanitized meat. [20a-20g] This can also be used to sanitize vegetables and other foods. [21a,21b] Farmers use this to cleanse the udders of cows to prevent mastitis, [22a,22b,22c] or to rid eggs of pathogenic bacteria. Chlorine dioxide can be used to disinfect endoscopes. [23a] Oxidants such as iodine, various peroxides, permanganate and chlorine dioxide can be applied topically to the skin to treat infections caused by bacteria or fungi. [24a-24d]

11)REDUCTANT RECOVERY SYSTEMS

Living things possess a recovery system to rescue oxidized sulfur compounds. It operates through donation of hydrogen atoms to these compounds and thereby restores their original condition as thiols. [59a,59b]

2 [H] + (GSSG) -> 2(GSH) This system is known as the hexose monophophate shunt. [59c,59d] A key player in this system is the enzyme glucose-6-phosphate-dehydrogenase (G6PDH). Patients with a genetic defect of G6PDH, known as glucose-6-phosphate-dehydrogenase deficiency disease, are especially sensitive to oxidants and to prooxidant drugs. However, this genetic disease has a benefit in that such individuals are naturally resistant to malaria. They can still catch malaria, but it is much less severe in them, since they permanently lack the enzyme necessary to assist the parasite in reactivating glutathione and other oxidized thiols. [60a-60h] Chlorine dioxide (ClO2) has been shown to oxidize and denature G6PDH by reaction with tyrosine and tryptophan residues inside the enzyme. [61a] Furthermore, G6PDH is sensitive to inhibition by sodium chlorate (NaClO3), another member of the chlorine oxide family of compounds. [61b,61c,61d] Sodium chlorate (NaClO3) is a trace ingredient present in the acicified sodium chlorite antimalarial solution. Some sodium chlorate (NaClO3) should also be produced in vivo by a slow reaction of chlorine dioxide (ClO2) with water under alkaline conditions [61e]. 2(ClO2) + 2(OH-) -> (ClO2-) + (ClO3-) + H2O

The Plasmodia may attempt to restore any thiols (RSH) lost to oxidation. However, this becomes more difficult as G6PDH is inhibited by chlorine dioxide (ClO2) or by chlorate (ClO3-).

12)SAFETY ISSUES

A remaining concern is safety. So far, at least anecdotally, the dosages of chlorine oxides as administered orally per the acidified sodium chlorite protocol have produced no definite toxicity. Some have taken this as often as 1 to 3 times weekly and on the surface seem to suffer no ill effects. To be certain if this is safe more research is warranted for such long term or repeated use. The concern is that too much or too frequent administration of oxidants could excessively deplete the body’s reductants and promote oxidative stress. One useful way to monitor this may be to periodically check methemoglobin levels in frequent users. Sodium chlorite, as found in municipal water supplies after disinfection by chorine dioxide, has been studied and proven safe. [79a-79i] Animal studies using much higher oral or topical doses have proven relatively safe. [80a-80p] In a suicide attempt 10g of sodium chlorite taken orally caused nearly fatal kidney failure and refractory methemoglobinemia. [81a] Inhalation or aerosol exposure to chlorine dioxide gas is highly irritating and generally not recommended. [82a-82g] Special precautions must be employed in cases of glucose-6-phosphate-dehydrogenase deficiency disease, as these patients are especially sensitive to oxidants of all kinds. [83a-83g] Nevertheless, oral acidified sodium chlorite solutions might even be found safe [84a,84b] and effective in them, but probably will need to be administered at lower doses.

13)SOME INCOMPATIBILITIES

Acidified sodium chlorite could provide a powerful new opportunity to improve or to restore sensitivity to quinolines by virtue of its oxidative power. However, quinolines contain secondary or tertiary amino groups which react with chlorine dioxide in such a way that both could destroy each other. Some possible strategies to resolve this incompatibility are suggested below.

1) Acidified sodium chlorite could be used as explained above only as a solo therapy.

2) Quinoline administration could be withheld until after the acidified sodium chorite has completed its action.

3) Patients already preloaded with a quinoline could stop this, wait a suitable period of time for this to wash out, then administer the acidified sodium chlorite.

4) The quinoline could remain in use and while the less active sodium chlorite is administered without acid. This should retain plenty of oxidant effectiveness without destroying any quinoline or wasting too much oxidant.

5) Switch from a quinoline to an endoperoxide (such as artemisinin) or to a quinone (such as atovaquone) before using acidified sodium chlorite, as these may be less sensitive toward destruction by chlorine dioxide.

Similar problems apply to methylene blue and many other drugs if they have an unoxidized sulfur atom, a phenol group, a secondary amine or a tertiary amine. Such are also very reactive with the chlorine dioxide component. [58a]

14)TARGETING IRON

While most available literature refers to redox imbalances causing depletion of necessary thiols, other mechanisms of toxicity of the oxides of chlorine against Plasmodia should also be considered. Oxides of chlorine are generally rapidly reactive with ferrous iron (Fe++) converting it to ferric (Fe+++). [62a-62d] This explains why in cases of overdosed exposures to oxides of chlorine such as sodium chlorite (NaClO2) there was a notable rise in methemoglobin levels. [63a,63b] Methemoglobin is a metabolically inactive form of hemoglobin in which its ferrous iron (Fe++) cofactor has been oxidized to ferric (Fe+++). In living things including parasites iron is a necessary cofactor for many enzymes. [64a-64f] Thus it is reasonable to expect that any damage to Plasmodia caused by oxides of chlorine is compounded by conversion of ferrous (Fe++) cofactors to ferric (Fe+++) or other alterations of iron compounds. [65a-65g] Superoxide dismutase (SOD) inside Plasmodial cells utilizes iron in its active center. [66a-66m] Chlorine dioxide also oxidizes manganese. [67a]

15)TARGETING POLYAMINES

Other metabolites necessary for survival and growth in tumors, bacteria and parasites are the polyamines. [68a-68d] Plasmodia quit growing and die, when polyamines are lacking [69a-69k], or when their functions are blocked [70a-70L]. Polyamines are also sensitive to oxidation and can be eliminated by strong oxidants. When oxidized, polyamines are converted to aldehydes, which are deadly to parasites and to tumors. [71a-71e] Chlorine dioxide (ClO2) is known to be especially reactive against secondary amines. [72a] This includes spermine and spermidine the two main biologically important polyamines. Thus any procedure which is successful to oxidize both thiols and polyamines does quadruple damage to the pathogen:

1) oxidation of the thiol ornithine decarboxylase inhibits polyamine synthesis;

2) oxidation of the thiol S-adenosyl-L-methionine decarboxylase also inhibits polyamine synthesis; (see references below and in “Targeting Thiols” above)

3) oxidation of the secondary amines spermidine and spermine depletes polyamine supplies;

4) the products of polyamine oxidation are toxic aldehydes.

16)TARGETING PROTEINS

Chlorine dioxide (ClO2) is highly reactive with thiols, phenols, secondary amines and tertiary amines. Therefore, proteins composed of amino acids which present these reactive groups are vulnerable to oxidation by this agent. Proteins which present residue(s) of the amino acid L-cysteine are discussed above under TARGETING THIOLS. L-tyrosine presents a phenol group and is therefore similarly vulnerable. L-tryptophan and L-histidine present secondary amino groups which are also especially reactive with chlorine dioxide. [78a-78d]

17)TARGETING PURINES

Purines are essential to many life processes. These molecules have a double ring structure. The rings are heterocyclic being composed of both carbon and nitrogen. Their nitrogen atoms are vulnerable to reaction with chlorine dioxide. [73a] Examples of important biologic purines are xanthine, hypoxanthine, inosine, guanine and adenine. Guanine and adenine are essential components of DNA and RNA necessary for all genetic functions and for all protein syntheses. Adenine is an essential component of the cofactors NADH, NADPH, FAD and ATP, necessary for many metabolic functions including oxidation-reduction and energy metabolism. Any purines lost by chlorine dioxide exposure can be readily replaced by host cells. [74a] Plasmodia and other apicomplexae are uniquely vulnerable to purine deficiency as they lack the enzymes necessary to produce purines for themselves [75a,75b,75c]. Instead these must be scavenged from host cells and imported across the plasma membranes of the parasite cells.

[76a-76i] Drugs are under development to inhibit purine utilization by Plasmodia and are already showing signs of success. [77a-77g] Temporarily destroying some of the purines in the blood as should occur upon brief exposure to chlorine dioxide in vivo is probably an additional stress that Plasmodia cannot tolerate.

18)TARGETING THIOLS

Like bacteria, fungi and tumor cells, the ability of Plasmodia to live and grow depends heavily on an internal abundance of reductants. This is especially true regarding thiol compounds also known as sulfhydryl compounds (RSH). [31a,31b] Thiols as a class behave as reductants (electron donors). As such they are especially sensitive to oxidants (electron grabbers). Thiols (RSH) such as glutathione [32a-32L] and other sulfur compounds [33a,33b,33c] are reactive with sodium chlorite (NaClO2) and with chlorine dioxide (ClO2). These are the very agents present in the acidified sodium chlorite solution. The products of oxidation of thiols (RSH) using various oxides of chlorine are: disulfides (RSSR), disulfide monoxides (RSSOR), sulfenic acids (RSOH), sulfinic acids (RSO2H), and sulfonic acids (RSO3H). None of these can support the life processes of the parasite. Upon sufficient removal of the parasite’s life sustaining thiols by oxidation, the parasite rapidly dies. [34a-34e] A list of thiols (RSH) upon which survival of Plasmodium species heavily depend includes: lipoic acid and dihydrolipoic acid [35a-35h], coenzyme A and acyl carrier protein [36a-36f], glutathione [37a-37m],glutathione reductase [38a-38e],glutathione-S-transferase [39a-39g], peroxiredoxin [40a-40L], thioredoxin [41a-41g], glutaredoxin [42a,42b,42c], plasmoredoxin [43a],thioredoxin reductase [44a-44g], falcipain [45a-45i],and ornithine decarboxylase [46a-46e].

▼Information

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8r. Modulation of monocyte chemokine production and nuclear factor kappa B activity by oxidants.Lee JS, Kahlon SS, Culbreth R, Cooper AD J Interferon Cytokine Res 1999 Jul;19(7):761-7B

8s. Intracellular glutathione redox status modulates MCP-1 expression in pulmonary granulomatous vasculitis.Desai A, Huang X, Warren JS Lab Invest 1999 Jul;79(7):837-47

8t. Nuclear factor kappa B: a pivotal role in the systemic inflammatory response syndrome and new target for therapy.Christman JW, Lancaster LH, Blackwell TS Intensive Care Med 1998 Nov;24(11):1131-8

Comment in: Intensive Care Med 1998 Nov;24(11):1129-30

8u. Differential regulation of extracellular signal-regulated kinase and nuclear factor-kappa B signal transduction pathways by hydrogen peroxide and tumor necrosis factor.Milligan SA, Owens MW, Grisham MB Arch Biochem Biophys 1998 Apr 15;352(2):255-62

8v. Hydrogen peroxide as a potent activator of T lymphocyte functions.Los M, Dröge W, Stricker K, Baeuerle PA, Schulze-Osthoff K Eur J Immunol 1995 Jan; 25(1):159-65

9a. Hydrogen Peroxide in Human Blood.Varma SD, Devamanoharan  See Radic Res Commun. 1991;14(2):125-31

9b. Histochemical demonstration of hydrogen peroxide production by leukocytes in fixed-frozen tissue sections of inflammatory lesions.Dannenberg AM Jr, Schofield BH, Rao JB, Dinh TT, Lee K,Boulay M, Abe Y, Tsuruta J, Steinbeck MJ J Leukoc Biol. 1994 Oct;56(4):436-43

9c. Interferon-gamma activates the oxidative killing of Candida albicans by human granulocytes.Stevenhagen A, van Furth R Clin Exp Immunol. 1993 Jan;91(1):170-5

9d. Hydrogen peroxide production by alveolar type II cells,alveolar macrophages, and endothelial cells.Kinnula VL, Everitt JI, Whorton AR, Crapo JD Am J Physiol. 1991 Aug;261(2 Pt 1):L84-91

9e. Stimulation of the respiratory burst and promotion of bacterial killing in human granulocytes by intravenous immunoglobulin preparations.Marodi L, Kalmar A, Karmazsin L Clin Exp Immunol. 1990 Feb;79(2):164-9

9f. Neutrophils may directly synthesize both H2O2 and O2- since surface stimuli induce their release in stimulus-specific ratios.Hoffstein ST, Gennaro DE, Manzi RM Inflammation. 1985 Dec;9(4):425-37

9g. Quantitative and temporal characterization of the extracellular H2O2 pool generated by human neutrophils.Test ST, Weiss SJ J Biol Chem. 1984 Jan 10;259(1):399-405

9h. Hydrogen peroxide release from eosinophils: quantitative,comparative studies of human and guinea pig eosinophils.Pincus SH J Invest Dermatol. 1983 Apr;80(4):278-81

9i. Pyridine nucleotide-dependent generation of hydrogen peroxide by a particulate fraction from human neutrophils.DeChatelet LR, Shirley PSJ  Immunol. 1981 Mar;126(3):1165-9

9j. Comparative studies on alveolar macrophages and polymorphonuclear leukocytes. I. H2O2 and O2- generation by rabbit alveolar macrophages.Yamaguchi T, Kakinuma K, Kaneda M, Shimada K J Biochem (Tokyo). 1980 May;87(5):1449-55

9k. Interrelationship between oxygen consumption,superoxide anion and hydrogen peroxide formation in phagocytosing guinea pig polymorphonuclear leucocytes.Dri P, Bellavite P, Berton G, Rossi F Mol Cell Biochem. 1979 Jan 26;23(2):109-22

9L. Hydrogen peroxide production and killing of Staphylococcus aureus by human polymorphonuclear leukocytes.Tsan MF, Douglass KH, McIntyre PA Blood. 1977 Mar;49(3):437-44

9m. The role of superoxide anion and hydrogen peroxide in phagocytosis-associated oxidative metabolic reactions.Baehner RL, Murrmann SK, Davis J, Johnston RB Jr J Clin Invest. 1975 Sep;56(3):571-6

9n. H2O2 release from human granulocytes during phagocytosis.I. Documentation, quantitation, and some regulating factors.Root RK, Metcalf J, Oshino N, Chance B J Clin Invest. 1975 May;55(5):945-55

9o. Production of hydrogen peroxide by phagocytizing human granulocytes.Homan-Muller JW, Weening RS, Roos D J Lab Clin Med. 1975 Feb;85(2):198-207

9p. Singlet excited oxygen as a mediator of the antibacterial action of leukocytes.Krinsky NI Science. 1974 Oct 25;186(4161):363-5

9q. Biological defense mechanisms. The production by leukocytes of superoxide, a potential bactericidal agent.Babior BM, Kipnes RS, Curnutte JT J Clin Invest. 1973 Mar;52(3):741-4

9r. The H2O2-production by polymorphonuclear leukocytes during phagocytosis.Zatti M, Rossi F, Patriarca P Experientia. 1968 Jul 15;24(7):669-70

9s. A new method for the detection of hydroxyl radical production by phagocytic cells.Sagone AL Jr, Decker MA, Wells RM, Democko C Biochim Biophys Acta. 1980 Feb 21;628(1):90-7

9t. Human granulocyte generation of hydroxyl radical.Weiss SJ, Rustagi PK, LoBuglio AF J Exp Med. 1978 Feb 1;147(2):316-23

9u. Production of singlet oxygen by eosinophils activated in vitro by C5a and leukotriene B4.Teixeira MM, Cunha FQ, Noronha-Dutra A, Hothersall J FEBS Lett. 1999 Jun 25;453(3):265-8

9v. Investigating antibody-catalyzed ozone generation by human neutrophils.Babior BM, Takeuchi C, Ruedi J, Gutierrez A, Wentworth P PNAS, Mar 18, 2003, 100(6):3031-3034

10a. Free radicals generation by granulocytes from men during bed rest.Pawlak W, Kedziora J, Zolynski K, Kedziora-Kornatowska K, Blaszczyk J, Witkowski P J Gravit Physiol. 1998 Jul;5(1):P131-2

10b. Eosinophils are a major source of nitric oxide-derived oxidants in severe asthma: characterization of pathways available to eosinophils for generating reactive nitrogen species.MacPherson JC, Comhair SA, Erzurum SC, Klein DF,Lipscomb MF, Kavuru MS, Samoszuk MK, Hazen SL J Immunol. 2001 May 1;166(9):5763-72

10c. Helicobacter pylori urease suppresses bactericidal activity of peroxynitrite via carbon dioxide production.Kuwahara H, Miyamoto Y, Akaike T, Kubota T, Sawa T,Okamoto S, Maeda H Infect Immun. 2000 Aug;68(8):4378-83

10d. Kinetics of nitric oxide and hydrogen peroxide production and formation of peroxynitrite during the respiratory burst of human neutrophils.Carreras MC, Pargament GA, Catz SD, Poderoso JJ, Boveris A FEBS Lett. 1994 Mar 14;341(1):65-8

10e. Biological aspects of reactive nitrogen species.Patel RP, McAndrew J, Sellak H, White CR, Jo H,Freeman BA, Darley-Usmar VM Biochim Biophys Acta. 1999 May 5;1411(2-3):385-400

10f. Peroxynitrite production by human neutrophils,monocytes and lymphocytes challenged with lipopolysaccharide.Gagnon C, Leblond FA, Filep JG FEBS Lett. 1998 Jul 10;431(1):107-10

10g. Superoxide and peroxynitrite generation from inducible nitric oxide synthase in macrophages.Xia Y, Zweier JL Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6954-8

10h. Peroxynitrite formation from activated human leukocytes.Fukuyama N, Ichimori K, Su Z, Ishida H, Nakazawa H Biochem Biophys Res Commun. 1996 Jul 16;224(2):414-9

11a. Chlorination of Taurine by Human Neutrophils –Evidence for Hypochlorous Acid Generation.Weiss SJ, Klein R, Slivka A, Wei M J Clin Invest, Sep 1982, 70:598-607

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12a. Human mononuclear phagocyte antiprotozoal mechanisms:oxygen-dependent vs oxygen-independent activity against intracellular Toxoplasma gondii.Murray HW, Rubin BY, Carriero SM, Harris AM, Jaffee EA J Immunol. 1985 Mar;134(3):1982-8

12b. Phagocytosis and killing of the protozoan Leishmania donovani by human polymorphonuclear leukocytes.Pearson RD, Steigbigel RT J Immunol. 1981 Oct;127(4):1438-43

12c. The role of the phagocyte in host-parasite interactions.The direct quantitative estimation of H2O2 in phagocytizing cells.Paul B, Sbarra AJ Biochim Biophys Acta. 1968 Feb 1;156(1):168-78

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13d. Treatment with oxidizing agents damages the inner membrane of spores of Bacillus subtilis and sensitizes spores to subsequent stress.Cortezzo DE, Koziol-Dube K, Setlow B, Setlow P J Appl Microbiol. 2004;97(4):838-52

14a. Mechanisms of killing of Bacillus subtilis spores by hypochlorite and chlorine dioxide.Young SB, Setlow P.J Appl Microbiol. 2003;95(1):54-67

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14c. The inhibitory effect of Alcide, an antimicrobial drug,on protein synthesis in Escherichia coli.Scatina J, Abdel-Rahman MS, Goldman E.J Appl Toxicol. 1985 Dec;5(6):388-94

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14f. Sporicidal properties of chlorine dioxide.Ridenour GM, Ingols RS, Armbruster EH Water & Sewage Works, 1949 96(8):1

14g. Efficacy of chlorine dioxide as a bacteriocide.Bernarde MA, Isreal BM, Olivieri VP, Granstrom ML Appl Microbiol, 1965, 13(5):776-780

14h. Kinetics and mechanism of bacterial disinfection by chlorine dioxide.Bernarde MA, Snow WB, Olivieri VP, Davidson B Appl Microbiol, 1967, 15(2):257-265

14i. Alternative Disinfectants and Oxidants EPA Guidance Manual, April 1999,4.4 Pathogen Inactivation and Disinfection Efficacy,pp 4-15 to 4-22

14j. Evaluation of ultrasonic scaling unit waterline contamination after use of chlorine dioxide mouth  rinse lavage.Wirthlin MR, Marshall GW JR J Periodontol. 2001 Mar;72(3):401-10

15a. Degradation of the Poliovirus 1 genome by chlorine dioxide.Simonet J, Gantzer C J Appl Microbiol. 2006 Apr;100(4):862-70

15b. Inactivation of enteric adenovirus and feline calicivirus by chlorine dioxide.Thurston-Enriquez JA, Haas CN, Jacangelo J, Gerba CP Appl Environ Microbiol. 2005 Jun;71(6):3100-5

15c. Mechanisms of inactivation of hepatitis A virus in water by chlorine dioxide.Li JW, Xin ZT, Wang XW, Zheng JL, Chao FH Water Res. 2004 Mar;38(6):1514-9

15d. Virucidal efficacy of four new disinfectants.Eleraky NZ, Potgieter LN, Kennedy MA J Am Anim Hosp Assoc. 2002 May-Jun;38(3):231-4

15e. Chlorine dioxide sterilization of red blood cells for transfusion, additional studies.Rubinstein A, Chanh T, Rubinstein DB. Int Conf AIDS. 1994 Aug 7-12; 10: 235 (abstract no. PB0953).U.S.C. School of Medicine, Los Angeles

15f. Inactivation of human immunodeficiency virus by a medical waste disposal process using chlorine dioxide.Farr RW, Walton C Infect Control Hosp Epidemiol. 1993 Sep;14(9):527-9

15g. Inactivation of human and simian rotaviruses by chlorine dioxide.Chen YS, Vaughn JM Appl Environ Microbiol. 1990 May;56(5):1363-6

15h. Disinfecting capabilities of oxychlorine compounds.Noss CI, Olivieri VP Appl Environ Microbiol. 1985 Nov;50(5):1162-4

15i. Mechanisms of inactivation of poliovirus by chlorine dioxide and iodine.Alvarez ME, O’Brien RT Appl Environ Microbiol. 1982 Nov;44(5):1064-71

15j. A comparison of the virucidal properties of chlorine,chlorine dioxide, bromine chloride and iodine.Taylor GR, Butler M J Hyg (Lond). 1982 Oct;89(2):321-8

15k. Inactivation of Poliomyelitis Virus by “Free” Chlorine.Ridennour GM, Ingols RS Am J Pub Health, 1946, 36(6):639

15L. Alternative Disinfectants and Oxidants EPA Guidance Manual, April 1999,4.4 Pathogen Inactivation and Disinfection Efficacy, pp 4-15 to 4-22

16a. Alternative Disinfectants and Oxidants EPA Guidance Manual, April 1999,4.4 Pathogen Inactivation and Disinfection Efficacy,pp 4-15 to 4-22

16b. Cysticidal effect of chlorine dioxide on Giardia intestinalis cysts.Winiecka-Krusnell J, Linder E Acta Trop. 1998 Jul 30;70(3):369-72

16c. Effects of ozone, chlorine dioxide, chlorine, and monochloramine on Cryptosporidium parvum oocyst viability.Korich DG, Mead JR, Madore MS, Sinclair NA, Sterling CR Appl Environ Microbiol. 1990 May;56(5):1423-8

16d. The effect of ‘Alcide’ on 4 strains of rodent coccidial oocysts.Owen DG Lab Anim. 1983 Oct;17(4):267-9

16e. Water Treatment and Pathogen Control –Process Efficiency in Achieving Safe Drinking Water.LeChevallier MW, Au KK Section 3.3.3 Chlorine dioxide pp 52-54 World Health Organization, IWA Publishing, 2004

16f. Sequential inactivation of Cryptosporidium parvum oocysts with chlorine dioxide followed by free chlorine or monochloramine.Corona-Vasquez B, Rennecker JL, Driedger AM, Mariñas BJ Water Res. 2002 Jan;36(1):178-88

17a. Disinfectant efficacy of chlorite and chlorine dioxide in drinking water biofilms.Gagnon GA, Rand JL, O’leary KC, Rygel AC, Chauret C, Andrews RC Water Research, 39(9):1809-17, May 2005

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17d. Disinfection: Water and Wastewater.Johnson JD Ann Arbor Science Publishers, Inc. 1975

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17h. Water Treatment and Pathogen Control –Process Efficiency in Achieving Safe Drinking Water.LeChevallier MW, Au KK Section 3.3.3 Chlorine dioxide pp 52-54 World Health Organization, IWA Publishing, 2004

17i. Matching odour treatment processes to odour resources.Jeavons J, Hodgson P, Upton J Water Science and Technology, 2000, 41(9):227-232

17j. The effect of predisinfection with chlorine dioxide on the formation of haloacetic acids and trihalomethanes in a drinking water supply.Harris CL Thesis submitted to Virginia Polytechnic Institute and State University, July 27,2001

17k. Effect of pH and temperature on the kinetics of odor oxidation using chlorine dioxide.Kastner JR, Das KC, Hu C, McClendon R J Air Waste Manag Assoc. 2003 Oct;53(10):1218-24

17L. Development of chlorine dioxide-related by-product models for drinking water treatment.Korn C, Andrew RC, Escobar MD Water Res. 2002 Jan;36(1):330-42

18a. Cadaverine as a putative component of oral malodor.Goldberg S, Kozlovsky A, Gordon D, Gelernter I,Sintov A, Rosenberg M J Dent Res. 1994 Jun;73(6):1168-72

18b. A multifactorial investigation of the ability of oral health care products (OHCPs) to alleviate oral malodour.Silwood CJ, Grootveld MC, Lynch E J Clin Periodontol. 2001 Jul;28(7):634-41

18c. Use of 0.1% chlorine dioxide to inhibit the formation of morning volatile sulphur compounds (VSC).Peruzzo DC, Jandiroba PF, Nogueira Filho Gda R Braz Oral Res. 2007 Jan-Mar;21(1):70-4

18d. Use of chlorine dioxide mouthrinse as the ultrasonic scaling lavage reduces the viable bacteria in the generated aerosols.Wirthlin MR, Choi JH, Kye SB J West Soc Periodontol Periodontal Abstr. 2006;54(2):35-44

18e. Use of a novel group of oral malodor measurements to evaluate an anti-oral malodor mouthrinse (TriOralTM)in humans.Codipilly DP, Kaufman HW, Kleinberg I J Clin Dent. 2004;15(4):98-104

18f. The clinical and microbiological effects of a novel acidified sodium chlorite mouthrinse on oral bacterial mucosal infections.Fernandes-Naglik L, Downes J, Shirlaw P, Wilson R,Challacombe SJ, Kemp GK, Wade WG Oral Dis. 2001 Sep;7(5):276-80

18g. Efficacy of a chlorine dioxide-containing mouthrinse in oral malodor.Frascella J, Gilbert RD, Fernandez P, Hendler J Compend Contin Educ Dent. 2000 Mar;21(3):241-4, 246, 248 passim; quiz 256

18h. Odor reduction potential of a chlorine dioxide mouthrinse.Frascella J, Gilbert R, Fernandez P J Clin Dent. 1998;9(2):39-42

18i. Use of a metastabilized chlorous acid/chlorine dioxide formulation as a mouthrinse for plaque reduction.Goultschin J, Green J, Machtei E, Stabholz A, Brayer L,Schwartz Z, Sela MN, Soskolne A Isr J Dent Sci. 1989 Oct;2(3):142-7

19a. Use of chlorine dioxide for cannery sanitation and water conservation.Welch JL, Folinazzo JF Food Technology, 1959, 13(3):179-182

20a. Effects of Carcass Washing Systems on Campylobacter Contamination in Large Broiler Processing Plants by M P Bashor,Masters Thesis, North Carolina State University, Dec 2002

20b. Research Project Outline #4111,by C N Cutter, Penn State Univ, Nov 2005

20c. Validation of the use of organic acids and acidified sodium chlorite to reduce Escherichia coli O157 and Salmonella typhimurium in beef trim and ground beef in a simulated processing environment.by Harris K, Miller MF, Loneragan GH, Brashears MM.J Food Prot. 69(8):1802-7, Aug 2006

20d. Decreased dosage of acidified sodium chlorite reduces microbial contamination and maintains organoleptic qualities of ground beef products.Bosilevac JM, Shackelford SD, Fahle R, Biela T, Koohmaraie M.J Food Prot. 2004 Oct;67(10):2248-54

20e. The Evaluation of Antimicrobial Treatments for Poultry Carcasses European Commission Health & Consumer Protection Directorate-General, April 2003

20f. Determination of chlorate and chlorite and mutagenicity of seafood treated with aqueous chlorine dioxide.Kim J, Marshall MR, Du WX, Otwell WS, Wei CI J Agric Food Chem. 1999 Sep;47(9):3586-91

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21a. Review – Application of Acidified Sodium Chlorite to Improve the Food Hygiene of Lightly Fermented Vegetables.by Y Inatsu, L Bari, S Kawamoto JARC 41(1 , pp 17-23, 2007

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22a. Efficacy of Two Barrier Teat Dips Containing Chlorous Acid Germicides Against Experimental Challenge …by R L Boddie, S C Nickerson, G K Kemp Journal of Dairy Science, 77 (10):3192-3197, 1994

22b. Evaluation of a Chlorous Experimental and Natural Acid Chlorine Dioxide Teat Dip Under Experimental and Natural Exposure Conditions by P A Drechsler, E E Wildman, J W Pankey Journal of Dairy Science, 73 (8):2121, 1990

22c. Preventing Bovine Mastitis by a Postmilking Teat Disinfectant Containing Acidified Sodium Chloriteby J E Hillerton, J Cooper, J Morelli Journal of Dairy Science, 90:1201-1208, 2007

23a. Endoscope disinfection using chlorine dioxide in an automated washer-disinfector.Isomoto H, Urata M, Kawazoe K, Matsuda J, Nishi Y, Wada A, Ohnita K, Hirakata Y, Matsuo N, Inoue K, Hirayama T,Kamihira S, Kohno S J Hosp Infect. 2006 Jul;63(3):298-305

24a. Clinical and microbiological efficacy of chlorine dioxide in the management of chronic atrophic candidiasis: an open study.Mohammad AR, Giannini PJ, Preshaw PM, Alliger H.Int Dent J. 2004 Jun;54(3):154-8

24b. Using a chlorine dioxide antibacterial gel for soft tissue healing.Babad MS Dent Today. 1999 Jun;18(6):88-9

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25a. Double-drug development against antioxidant enzymes from Plasmodium falciparum. Biot C, Dessolin J, Grellier P, Davioud-Charvet E Redox Rep. 2003;8(5):280-3

25b. Oxidative stress and antioxidant defenses: a target for the treatment of diseases caused by parasitic protozoa.Turrens JF Mol Aspects Med. 2004 Feb-Apr;25(1-2):211-20

25c. Vampires, Pasteur and reactive oxygen species. Is the switch from aerobic to anaerobic metabolism a preventive antioxidant defence in blood-feeding parasites?Oliveira PL, Oliveira MF FEBS Lett. 2002 Aug 14;525(1-3):3-6

25d. The role of cell-mediated immune responses in resistance to malaria, with special reference to oxidant stress.Allison AC, Eugui EM Annu Rev Immunol. 1983;1:361-92

25e. Thalassaemia trait, red blood cell age and oxidant stress: effects on Plasmodium falciparum growth and sensitivity to artemisinin.Senok AC, Nelson EA, Li K, Oppenheimer SJ Trans R Soc Trop Med Hyg. 1997 Sep-Oct;91(5):585-9

25f. Antiplasmodial activity of nitroaromatic and quinoidal compounds: redox potential vs. inhibition of erythrocyte glutathione reductase.Grellier P, Sarlauskas J, Anusevicius Z, Maroziene A,Houee-Levin C, Schrevel J, Cenas N Arch Biochem Biophys. 2001 Sep 15;393(2):199-206

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26a. Mechanism-based design of parasite-targeted artemisinin derivatives: synthesis and antimalarial activity of new diamine containing analogues.Hindley S, Ward SA, Storr RC, Searle NL, Bray PG, Park BK,Davies J, O’Neill PM J Med Chem. 2002 Feb 28;45(5):1052-63

26b. Proposed reductive metabolism of artemisinin by glutathione transferases in vitro.Mukanganyama S, Naik YS, Widersten M, Mannervik B,Hasler JA Free Radic Res. 2001 Oct;35(4):427-34

26c. Effect of dihydroartemisinin on the antioxidant capacity of P. falciparum-infected erythrocytes.Ittarat W, Sreepian A, Srisarin A, Pathepchotivong K Southeast Asian J Trop Med Public Health. 2003 Dec;34(4):744-50

26d. Evidence that haem iron in the malaria parasite is not needed for the antimalarial effects of artemisinin.Parapini S, Basilico N, Mondani M, Olliaro P,Taramelli D, Monti D FEBS Lett. 2004 Sep 24;575(1-3):91-4

26e. Why artemisinin and certain synthetic peroxides are potent antimalarials. Implications for the mode of action.Jefford CW Curr Med Chem. 2001 Dec;8(15):1803-26

26f. Redox reaction of artemisinin with ferrous and ferric ions in aqueous buffer.Sibmooh N, Udomsangpetch R, Kujoa A, Chantharaksri U,Mankhetkorn S Chem Pharm Bull (Tokyo). 2001 Dec;49(12):1541-6

26g. Artemisinin and the antimalarial endoperoxides: from herbal remedy to targeted chemotherapy.Meshnick SR, Taylor TE, Kamchonwongpaisan S Microbiol Rev. 1996 Jun;60(2):301-15

26h. The mode of action of antimalarial endoperoxides. Meshnick SR Trans R Soc Trop Med Hyg. 1994 Jun;88 Suppl 1:S31

26i. Iron-dependent free radical generation from the antimalarial agent artemisinin (qinghaosu).Meshnick SR, Yang YZ, Lima V, Kuypers F,Kamchonwongpaisan S, Yuthavong Y Antimicrob Agents Chemother. 1993 May;37(5):1108-14

26j. Effect of beta-arteether treatment on erythrocytic methemoglobin reductase system in Plasmodium yoelii nigeriensis infected mice. Srivastava S, Alhomida AS, Siddiqi NJ, Pandey VC, Puri SK Drug Chem Toxicol. 2001 May;24(2):181-90

26k. In vitro assessment of methylene blue on chloroquine-sensitive and -resistant Plasmodium falciparum strains reveals synergistic action with artemisinins.Akoachere M, Buchholz K, Fischer E, Burhenne J,Haefeli WE, Schirmer RH, Becker K Antimicrob Agents Chemother. 2005 Nov;49(11):4592-7

26L. Studies on hepatic oxidative stress and antioxidant defence systems during arteether treatment of Plasmodium yoelii nigeriensis infected mice.Siddiqi NJ, Pandey VC Mol Cell Biochem. 1999 Jun;196(1-2):169-73

26m. Effect of sodium artesunate on malaria infected human erythrocytes.Pan HZ, Lin FB, Zhang ZA Proc Chin Acad Med Sci Peking Union Med Coll. 1989;4(4):181-5

27a. Radical-mediated damage to parasites and erythrocytes in Plasmodium vinckei infected mice after injection of t-butyl hydroperoxide.Clark IA, Hunt NH, Cowden WB, Maxwell LE, Mackie EJ Clin Exp Immunol. 1984 Jun;56(3):524-30

28a. Potentiation of an antimalarial oxidant drug.Winter RW, Ignatushchenko M, Ogundahunsi OA,Cornell KA, Oduola AM, Hinrichs DJ, Riscoe MK Antimicrob Agents Chemother. 1997 Jul;41(7):1449-54

29a. The multiple roles of the mitochondrion of the malarial parasite.Krungkrai J Parasitology. 2004 Nov;129(Pt 5):511-24

29b. Antimalarial quinones: redox potential dependence of methemoglobin formation and heme release in erythrocytes.Lopez-Shirley K, Zhang F, Gosser D, Scott M, Meshnick SR J Lab Clin Med. 1994 Jan;123(1):126-30

29c. Antimalarial efficacy of methylene blue and menadione and their effect on glutathione metabolism of Plasmodium yoelii-infected albino mice.Arora K, Srivastava AK Parasitol Res. 2005 Dec;97(6):521-6

29d. Antiplasmodial activity of nitroaromatic and quinoidal compounds: redox potential vs. inhibition of erythrocyte glutathione reductase.Grellier P, Sarlauskas J, Anusevicius Z, Maroziene A,Houee-Levin C, Schrevel J, Cenas N Arch Biochem Biophys. 2001 Sep 15;393(2):199-206

29e. Antiplasmodial activity of naphthoquinones related to lapachol and beta-lapachone.Perez-Sacau E, Estevez-Braun A, Ravelo AG,Gutierrez Yapu D, Gimenez Turba A Chem Biodivers. 2005 Feb;2(2):264-74

29f. Newbouldiaquinone A: A naphthoquinone-anthraquinone ether coupled pigment, as a potential antimicrobial and antimalarial agent from Newbouldia laevis.Eyong KO, Folefoc GN, Kuete V, Beng VP, Krohn K, Hussain H,Nkengfack AE, Saeftel M, Sarite SR, Hoerauf A Phytochemistry. 2006 Mar;67(6):605-9;Epub 2006 Jan 26

29g. Anthranoid compounds with antiprotozoal activity from Vismia orientalis.Mbwambo ZH, Apers S, Moshi MJ, Kapingu MC, Van Miert S,Claeys M, Brun R, Cos P, Pieters L, Vlietinck A Planta Med. 2004 Aug;70(8):706-10

29h. Antimalarial activity of phenazines from lapachol, beta-lapachone and its derivatives against Plasmodium falciparum in vitro and Plasmodium berghei in vivo.de Andrade-Neto VF, Goulart MO, da Silva Filho JF,da Silva MJ, Pinto Mdo C, Pinto AV, Zalis MG,Carvalho LH, Krettli AU Bioorg Med Chem Lett. 2004 Mar 8;14(5):1145-9

29i. In vitro antiprotozoal and cytotoxic activities of some alkaloids, quinones, flavonoids, and coumarins.del Rayo Camacho M, Phillipson JD, Croft SL, Yardley V,Solis PN Planta Med. 2004 Jan;70(1):70-2

29j. Aminonaphthoquinones–a novel class of compounds with potent antimalarial activity against Plasmodium falciparum.Kapadia GJ, Azuine MA, Balasubramanian V, Sridhar R Pharmacol Res. 2001 Apr;43(4):363-7

29k. In vitro response of Plasmodium falciparum to atovaquone and correlation with other antimalarials: comparison between African and Asian strains.Gay F, Bustos D, Traore B, Jardinel C, Southammavong M,Ciceron L, Danis MM Am J Trop Med Hyg. 1997 Mar;56(3):315-7

29L. In vitro activity of natural and synthetic naphthoquinones against erythrocytic stages of Plasmodium falciparum.Carvalho LH, Rocha EM, Raslan DS, Oliveira AB, Krettli AUBraz J Med Biol Res. 1988;21(3):485-7

29m. Antiplasmodial and antioxidant isofuranonaphthoquinones from the roots of Bulbine capitata.Bezabih M, Abegaz BM, Dufall K, Croft K, Skinner-Adams T,Davis TM Planta Med. 2001 Jun;67(4):340-4

30a. Methylene blue as an antimalarial agent. Schirmer RH, Coulibaly B, Stich A, Scheiwein M,Merkle H, Eubel J, Becker K, Becher H, Müller O,Zich T, Schiek W, Kouyaté B Redox Rep. 2003;8(5):272-5

30b. Recombinant Plasmodium falciparum glutathione reductase is inhibited by the antimalarial dye methylene blue.Farber PM, Arscott LD, Williams CH Jr, Becker K,Schirmer RH FEBS Lett. 1998 Feb 6;422(3):311-4

30c. Antimalarial efficacy of methylene blue and menadione and their effect on glutathione metabolism of Plasmodium yoelii-infected albino mice.Arora K, Srivastava AK Parasitol Res. 2005 Dec;97(6):521-6

30d. Methylene blue for malaria in Africa: results from a dose-finding study in combination with chloroquine Meissner PE, Mandi G, Coulibaly B, Witte S, Tapsoba T,Mansmann U, Rengelshausen J, Schiek W, Jahn A,Walter-Sack I, Mikus G, Burhenne J, Riedel KD,Schirmer RH, Kouyaté B, Müller O Malar J. 2006;5:84

30e. In vitro assessment of methylene blue on chloroquine-sensitive and -resistant Plasmodium falciparum strains reveals synergistic action with artemisinins.Akoachere M, Buchholz K, Fischer E, Burhenne J,Haefeli WE, Schirmer RH, Becker K Antimicrob Agents Chemother. 2005 Nov;49(11):4592-7

30f. Mode of antimalarial effect of methylene blue and some of its analogues on Plasmodium falciparum in culture and their inhibition of P. vinckei petteri and P. yoelii nigeriensis in vivo.Atamna H, Krugliak M, Shalmiev G, Deharo E,Pescarmona G, Ginsburg H Biochem Pharmacol. 1996 Mar 8;51(5):693-700

30g. Antimalarial dyes revisited: xanthenes, azines, oxazines, and thiazines.Vennerstrom JL, Makler MT, Angerhofer CK, Williams JA Antimicrob Agents Chemother. 1995 Dec;39(12):2671-7

30h. The influence of methylene blue on the pentose phosphate pathway in erythrocytes of monkeys infected with Plasmodium knowlesi.Barnes MG, Polet H J Lab Clin Med. 1969 Jul;74(1):1-11

30i. The phenothiazinium chromophore and the evolution of antimalarial drugs.Wainwright M, Amaral L Trop Med Int Health. 2005 Jun;10(6):501-11

31a. Thiol-based redox metabolism of protozoan parasites.Muller S, Liebau E, Walter RD, Krauth-Siegel RL Trends Parasitol. 2003 Jul;19(7):320-8 Comment in: Trends Parasitol. 2004 Feb;20(2):58-9

31b. Glutathione, altruistic metabolite in fungi.Pócsi I, Prade RA, Penninckx MJ Adv Microb Physiol. 2004;49:1-76

32a. A comparison of the effects of ocular preservatives on mammalian and microbial ATP and glutathione levels.Ingram PR, Pitt AR, Wilson CG, Olejnik O, Spickett CM Free Radic Res. 2004 Jul;38(7):739-50

32b. The effect of Alcide, a new antimicrobial drug, on rat blood glutathione and erythrocyte osmotic fragility, in vitro.Abdel-Rahman MS, Scatina J J Appl Toxicol. 1985 Jun;5(3):178-81

32c. Chlorite-hemoprotein interaction as key role for the pharmacological activity of the chlorite-based drug WF10.Schempp H, Reim M, Dornisch K, Elstner EF Arzneimittelforschung. 2001;51(7):554-62

32d. Kinetics and mechanisms of chlorine dioxide and chlorite oxidations of cysteine and glutathione.Ison A, Odeh IN, Margerum DW Inorg Chem. 2006 Oct 16;45(21):8768-75

32e. The interaction of sodium chlorite with phospholipids and glutathione: a comparison of effects in vitro, in mammalian and in microbial cells.Ingram PR, Homer NZ, Smith RA, Pitt AR, Wilson CG, Olejnik O, Spickett CM Arch Biochem Biophys. 2003 Feb 1;410(1):121-33

32f. Pharmacodynamics of alcide, a new antimicrobial compound, in rat and rabbit.Scatina J, Abdel-Rahman MS, Gerges SE, Khan MY, Gona O Fundam Appl Toxicol. 1984 Jun;4(3 Pt 1):479-84(decreased glutathion)

32g. Effect of chlorine dioxide and metabolites on glutathione dependent system in rat, mouse and chicken blood.Couri D, Abdel-Rahman MS J Environ Pathol Toxicol 1979 Dec;3(1-2):451-60

32h. Kinetics of Cl02 and effects of Cl02, Cl02-, and Cl03- in drinking water on blood glutathione and hemolysis in rat and chicken.Abdel-Rahman MS, Couri D, Bull RJ J Environ Pathol Toxicol. 1979 Dec;3(1-2):431-49

32i. Oxidative damage to the erythrocyte induced by sodium chlorite, in vitro.Heffernan WP, Guion C, Bull RJ J Environ Pathol Toxicol. 1979 Jul-Aug;2(6):1501-10(chlorite depletes GSH)

32j. Oxidative damage to the erythrocyte induced by sodium chlorite, in vivo.Heffernan WP, Guion C, Bull RJ J Environ Pathol Toxicol. 1979 Jul-Aug;2(6):1487-99 (chlorite decreases GSH)

32k. The effect of Alcide, a new antimicrobial drug, on rat blood glutathione and erythrocyte osmotic fragility, in vitro.Abdel-Rahman MS, Scatina JJ Appl Toxicol. 1985 Jun;5(3):178-81

32L. Toxicity of chlorine dioxide in drinking water.Abdel-Rahman MS, Couri D, Bull RJ J Environ Pathol Toxicol Oncol. 1985 Sep-Oct;6(1):105-13

33a. Oxyhalogen-Sulfur Chemistry: Kinetics and Mechanism of Oxidation of N-Acetylthiourea by Chlorite and Chlorine Dioxide.Olagunju O, Siegel PD, Olojo R, Simoyi RH J Phys Chem A, 110 (7), 2396 -2410, 2006

33b. Oxyhalogen-Sulfur Chemistry: Oxidation of N-Acetylcysteine by Chlorite and Acidic Bromate.Darkwa J, Olojo R, Olagunju O, Otoikhian A, Simoyi RH J. Phys. Chem. A, 107 (46), 9834 -9845, 2003

33c. Oxyhalogen – Sulfur Chemistry: Oxidation of Taurine by Chlorite in Acidic Medium Chinake CR, Simoyi RH J Phys Chem B, 1997, 101, 1207

34a. Thioredoxin networks in the malarial parasite Plasmodium falciparum.Nickel C, Rahlfs S, Deponte M, Koncarevic S, Becker K Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1227-39

34b. Thioredoxin and glutathione system of malaria parasite Plasmodium falciparum.Muller S, Gilberger TW, Krnajski Z, Luersen K, Meierjohann S, Walter RD, Muller S, Lüersen K Protoplasma. 2001;217(1-3):43-9

34c. Plasmodium falciparum thioredoxins and glutaredoxins as central players in redox metabolism.Rahlfs S, Nickel C, Deponte M, Schirmer RH, Becker K Redox Rep. 2003;8(5):246-50

34d. The thiol-based redox networks of pathogens: unexploited targets in the search for new drugs.Jaeger T, Flohe L, Flohé L Biofactors. 2006;27(1-4):109-20

34e. Redox and antioxidant systems of the malaria parasite Plasmodium falciparum.Muller S Mol Microbiol. 2004 Sep;53(5):1291-305

35a. The plasmodial apicoplast was retained under evolutionary selective pressure to assuage blood stage oxidative stress.Toler SMed Hypotheses. 2005;65(4):683-90

35b. Scavenging of the cofactor lipoate is essential for the survival of the malaria parasite Plasmodium falciparum Allary M, Lu JZ, Zhu L, Prigge ST Mol Microbiol. 2007 Mar;63(5):1331-44;Epub 2007 Jan 22

35c. Plasmodium falciparum possesses organelle-specific alpha-keto acid dehydrogenase complexes and lipoylation pathways.Günther S, McMillan PJ, Wallace LJ, Müller S Biochem Soc Trans. 2005 Nov;33(Pt 5):977-80

35d. The malaria parasite Plasmodium falciparum has only one pyruvate dehydrogenase complex, which is located in the apicoplast.Foth BJ, Stimmler LM, Handman E, Crabb BS, Hodder AN, McFadden GI Mol Microbiol. 2005 Jan;55(1):39-53 Comment in: Mol Microbiol. 2005 Jan;55(1):1-4

35e. The human malaria parasite Plasmodium falciparum possesses two distinct dihydrolipoamide dehydrogenases.McMillan PJ, Stimmler LM, Foth BJ, McFadden GI, Müller S Mol Microbiol. 2005 Jan;55(1):27-38Comment in: Mol Microbiol. 2005 Jan;55(1):1-4

35f. The human malaria parasite Plasmodium falciparum has distinct organelle-specific lipoylation pathways.Wrenger C, Müller S Mol Microbiol. 2004 Jul;53(1):103-13

35g. Apicomplexan parasites contain a single lipoic acid synthase located in the plastid.Thomsen-Zieger N, Schachtner J, Seeber F FEBS Lett. 2003 Jul 17;547(1-3):80-6

35h. Biosynthetic pathways of plastid-derived organelles as potential drug targets against parasitic apicomplexa.Seeber F Curr Drug Targets Immune Endocr Metabol Disord. 2003 Jun;3(2):99-109

36a. Fatty acid biosynthesis as a drug target in apicomplexan parasites.Goodman CD, McFadden GI Curr Drug Targets. 2007 Jan;8(1):15-30

36b. Apicoplast fatty acid biosynthesis as a target for medical intervention in apicomplexan parasites.Gornicki P Int J Parasitol. 2003 Aug;33(9):885-96

36c. A type II pathway for fatty acid biosynthesis presents drug targets in Plasmodium falciparum.Waller RF, Ralph SA, Reed MB, Su V, Douglas JD, Minnikin DE, Cowman AF, Besra GS, McFadden GI Antimicrob Agents Chemother. 2003 Jan;47(1):297-301

36d. Recombinant expression and biochemical characterization of the unique elongating beta-ketoacyl-acyl carrier protein synthase involved in fatty acid biosynthesis of Plasmodium falciparum using natural and artificial substrates Lack G, Homberger-Zizzari E, Folkers G, Scapozza L, Perozzo R J Biol Chem. 2006 Apr 7;281(14):9538-46

36e. Identification, characterization, and inhibition of Plasmodium falciparum beta-hydroxyacyl-acyl carrier protein dehydratase (FabZ).Sharma SK, Kapoor M, Ramya TN, Kumar S, Kumar G, Modak R, Sharma S, Surolia N, Surolia A J Biol Chem. 2003 Nov 14;278(46):45661-71

36f. Analyses of co-operative transitions in Plasmodium falciparum beta-ketoacyl acyl carrier protein reductase upon co-factor and acyl carrier protein binding.Karmodiya K, Surolia N FEBS J. 2006 Sep;273(17):4093-103

37a. Characterization of the glyoxalases of the malarial parasite Plasmodium falciparum and comparison with their human counterparts Akoachere M, Iozef R, Rahlfs S, Deponte M, Mannervik B, Creighton DJ, Schirmer H, Becker K Biol Chem. 2005 Jan;386(1):41-52

37b. Glutathione–functions and metabolism in the malarial parasite Plasmodium falciparum.Becker K, Rahlfs S, Nickel C, Schirmer RH Biol Chem. 2003 Apr;384(4):551-66

37c. The thioredoxin system of the malaria parasite Plasmodium falciparum. Glutathione reduction revisited.Kanzok SM, Schirmer RH, Turbachova I, Iozef R, Becker K J Biol Chem. 2000 Dec 22;275(51):40180-6

37d. Thioredoxin and glutathione system of malaria parasite Plasmodium falciparum.Muller S, Gilberger TW, Krnajski Z, Luersen K, Meierjohann S, Walter RD, Muller S, Lüersen K Protoplasma. 2001;217(1-3):43-9

37e. Thioredoxin reductase and glutathione synthesis in Plasmodium falciparum.Muller S, Muller S Redox Rep. 2003;8(5):251-5

37f. Plasmodium falciparum-infected red blood cells depend on a functional glutathione de novo synthesis attributable to an enhanced loss of glutathione.Luersen K, Walter RD, Muller S, LÃersen K, MÃller S Biochem J. 2000 Mar 1;346 Pt 2:545-52

37g. Characterization of the glyoxalases of the malarial parasite Plasmodium falciparum and comparison with their human counterparts.Akoachere M, Iozef R, Rahlfs S, Deponte M, Mannervik B, Creighton DJ, Schirmer H, Becker K Biol Chem. 2005 Jan;386(1):41-52

37h. Glutathione synthetase from Plasmodium falciparum.Meierjohann S, Walter RD, Muller S Biochem J. 2002 May 1;363(Pt 3):833-8

37i. Ceramide mediates growth inhibition of the Plasmodium falciparum parasite.Pankova-Kholmyansky I, Dagan A, Gold D, Zaslavsky Z, Skutelsky E, Gatt S, Flescher E Cell Mol Life Sci. 2003 Mar;60(3):577-87

37j. The malaria parasite supplies glutathione to its host cell–investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum.Atamna H, Ginsburg H Eur J Biochem. 1997 Dec 15;250(3):670-9

37k. Redox processes in malaria and other parasitic diseases. Determination of intracellular glutathione.Becker K, Gui M, Traxler A, Kirsten C, Schirmer RH Histochemistry. 1994 Nov;102(5):389-95

37L. The effect of Alcide, a new antimicrobial drug, on rat blood glutathione and erythrocyte osmotic fragility, in vitro.Abdel-Rahman MS, Scatina J J Appl Toxicol. 1985 Jun;5(3):178-81

37m. Toxicity of chlorine dioxide in drinking water.Abdel-Rahman MS, Couri D, Bull RJ J Environ Pathol Toxicol Oncol. 1985 Sep-Oct;6(1):105-13

38a. Glutathione reductase-deficient erythrocytes as host cells of malarial parasites.Zhang Y, Konig I, Schirmer RH Biochem Pharmacol. 1988 Mar 1;37(5):861-5

38b. Glutathione reductase of the malarial parasite Plasmodium falciparum: crystal structure and inhibitor development.Sarma GN, Savvides SN, Becker K, Schirmer M, Schirmer RH, Karplus PA J Mol Biol. 2003 May 9;328(4):893-907

38c. Kinetic characterization of glutathione reductase from the malarial parasite Plasmodium falciparum. Comparison with the human enzyme.Bohme CC, Arscott LD, Becker K, Schirmer RH, Williams CH Jr J Biol Chem. 2000 Dec 1;275(48):37317-23

38d. Glutathione reductase inhibitors as potential antimalarial drugs. Effects of nitrosoureas on Plasmodium falciparum in vitro.Zhang YA, Hempelmann E, Schirmer RH Biochem Pharmacol. 1988 Mar 1;37(5):855-60

38e. Glutathione reductase inhibitors as potential antimalarial drugs. Effects of nitrosoureas on Plasmodium falciparum in vitro.Zhang YA, Hempelmann E, Schirmer RH Biochem Pharmacol. 1988 Mar 1;37(5):855-60

39a. Glutathione S-transferase of the malarial parasite Plasmodium falciparum: characterization of a potential drug target.Harwaldt P, Rahlfs S, Becker K Biol Chem. 2002 May;383(5):821-30

39b. Glutathione S-transferase from malarial parasites: structural and functional aspects.Deponte M, Becker K Methods Enzymol. 2005;401:241-53

39c. The glutathione S-transferase from Plasmodium falciparum.Liebau E, Bergmann B, Campbell AM, Teesdale-Spittle P, Brophy PM, Larsen K, Walter RD Mol Biochem Parasitol. 2002 Sep-Oct;124(1-2):85-90

39d. Glutathione S-transferases and related proteins from pathogenic human parasites behave as immunomodulatory factors.Ouaissi A, Ouaissi M, Sereno D Immunol Lett. 2002 May 1;81(3):159-64

39e. Plasmodium falciparum glutathione S-transferase–structural and mechanistic studies on ligand binding and enzyme inhibition.Hiller N, Fritz-Wolf K, Deponte M, Wende W, Zimmermann H, Becker K Protein Sci. 2006 Feb;15(2):281-9

39f. Cooperativity and pseudo-cooperativity in the glutathione S-transferase from Plasmodium falciparum.Liebau E, De Maria F, Burmeister C, Perbandt M, Turella P, Antonini G, Federici G, Giansanti F, Stella L, Lo Bello M, Caccuri AM, Ricci G J Biol Chem. 2005 Jul 15;280(28):26121-8

39g. X-ray structure of glutathione S-transferase from the malarial parasite Plasmodium falciparum.Fritz-Wolf K, Becker A, Rahlfs S, Harwaldt P, Schirmer RH, Kabsch W, Becker K Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):13821-6

40a. Roles of 1-Cys peroxiredoxin in haem detoxification in the human malaria parasite Plasmodium falciparum.Kawazu S, Ikenoue N, Takemae H, Komaki-Yasuda K, Kano S FEBS J. 2005 Apr;272(7):1784-91

40b. Structural and biochemical characterization of a mitochondrial peroxiredoxin from Plasmodium falciparum.Boucher IW, McMillan PJ, Gabrielsen M, Akerman SE, Brannigan JA, Schnick C, Brzozowski AM, Wilkinson AJ, Muller S, Müller S Mol Microbiol. 2006 Aug;61(4):948-59

40c. 2-Cys Peroxiredoxin TPx-1 is involved in gametocyte development in Plasmodium berghei.Yano K, Komaki-Yasuda K, Tsuboi T, Torii M, Kano S, Kawazu S Mol Biochem Parasitol. 2006 Jul;148(1):44-51

40d. Plasmodium falciparum 2-Cys peroxiredoxin reacts with plasmoredoxin and peroxynitrite.Nickel C, Trujillo M, Rahlfs S, Deponte M, Radi R, Becker K Biol Chem. 2005 Nov;386(11):1129-36

40e. Expression of mRNAs and proteins for peroxiredoxins in Plasmodium falciparum erythrocytic stage.Yano K, Komaki-Yasuda K, Kobayashi T, Takemae H, Kita K, Kano S, Kawazu S Parasitol Int. 2005 Mar;54(1):35-41

40f. Crystal structure of a novel Plasmodium falciparum 1-Cys peroxiredoxin.Sarma GN, Nickel C, Rahlfs S, Fischer M, Becker K, Karplus PA J Mol Biol. 2005 Mar 4;346(4):1021-34

40g. 2-Cys peroxiredoxin PfTrx-Px1 is involved in the antioxidant defence of Plasmodium falciparum.Akerman SE, Muller S, Müller S Mol Biochem Parasitol. 2003 Aug 31;130(2):75-81

40h. Expression profiles of peroxiredoxin proteins of the rodent malaria parasite Plasmodium yoelii.Kawazu S, Nozaki T, Tsuboi T, Nakano Y, Komaki-Yasuda K, Ikenoue N, Torii M, Kano S Int J Parasitol. 2003 Nov;33(13):1455-61

40i. Disruption of the Plasmodium falciparum 2-Cys peroxiredoxin gene renders parasites hypersensitive to reactive oxygen and nitrogen species.Komaki-Yasuda K, Kawazu S, Kano S FEBS Lett. 2003 Jul 17;547(1-3):140-4

40j. Molecular characterization of a 2-Cys peroxiredoxin from the human malaria parasite Plasmodium falciparum.Kawazu S, Komaki K, Tsuji N, Kawai S, Ikenoue N, Hatabu T, Ishikawa H, Matsumoto Y, Himeno K, Kano S Mol Biochem Parasitol. 2001 Aug;116(1):73-9

40k. Isolation and functional analysis of two thioredoxin peroxidases (peroxiredoxins) from Plasmodium falciparum.Krnajski Z, Walter RD, Muller S, Müller S Mol Biochem Parasitol. 2001 Apr 6;113(2):303-8

40L. Thioredoxin peroxidases of the malarial parasite Plasmodium falciparum.Rahlfs S, Becker KEur J Biochem. 2001 Mar;268(5):1404-9

41a. The thioredoxin system of the malaria parasite Plasmodium falciparum. Glutathione reduction revisited.Kanzok SM, Schirmer RH, Turbachova I, Iozef R, Becker K J Biol Chem. 2000 Dec 22;275(51):40180-6

41b. Thioredoxin networks in the malarial parasite Plasmodium falciparum.Nickel C, Rahlfs S, Deponte M, Koncarevic S, Becker K Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1227-39

41c. Thioredoxin and glutathione system of malaria parasite Plasmodium falciparum.Muller S, Gilberger TW, Krnajski Z, Luersen K, Meierjohann S, Walter RD, Muller S, Lüersen K Protoplasma. 2001;217(1-3):43-9

41d. Thioredoxin reductase and glutathione synthesis in Plasmodium falciparum.Muller S, Muller S Redox Rep. 2003;8(5):251-5

41e. Plasmodium falciparum thioredoxins and glutaredoxins as central players in redox metabolism.Rahlfs S, Nickel C, Deponte M, Schirmer RH, Becker K Redox Rep. 2003;8(5):246-50

41f. The thioredoxin system of Plasmodium falciparum and other parasites.Rahlfs S, Schirmer RH, Becker K Cell Mol Life Sci. 2002 Jun;59(6):1024-41

41g. Thioredoxin, thioredoxin reductase, and thioredoxin peroxidase of malaria parasite Plasmodium falciparum.Kanzok SM, Rahlfs S, Becker K, Schirmer RH Methods Enzymol. 2002;347:370-81

42a. Plasmodium falciparum thioredoxins and glutaredoxins as central players in redox metabolism.Rahlfs S, Nickel C, Deponte M, Schirmer RH, Becker K Redox Rep. 2003;8(5):246-50

42b. Plasmodium falciparum possesses a classical glutaredoxin and a second, glutaredoxin-like protein with a PICOT homology domain.Rahlfs S, Fischer M, Becker K J Biol Chem. 2001 Oct 5;276(40):37133-40

42c. Plasmodium falciparum glutaredoxin-like proteins.Deponte M, Becker K, Rahlfs S Biol Chem. 2005 Jan;386(1):33-40

43a. Plasmoredoxin, a novel redox-active protein unique for malarial parasites.Becker K, Kanzok SM, Iozef R, Fischer M, Schirmer RH, Rahlfs S Eur J Biochem. 2003 Mar;270(6):1057-64

44a. Double-drug development against antioxidant enzymes from Plasmodium falciparum.Biot C, Dessolin J, Grellier P, Davioud-Charvet E Redox Rep. 2003;8(5):280-3

44b. Thioredoxin reductase and glutathione synthesis in Plasmodium falciparum.Muller S, Muller S Redox Rep. 2003;8(5):251-5

44c. Specific inhibitors of Plasmodium falciparum thioredoxin reductase as potential antimalarial agents.Andricopulo AD, Akoachere MB, Krogh R, Nickel C, McLeish MJ, Kenyon GL, Arscott LD, Williams CH Jr, Davioud-Charvet E, Becker K Bioorg Med Chem Lett. 2006 Apr 15;16(8):2283-92

44d. Thioredoxin, thioredoxin reductase, and thioredoxin peroxidase of malaria parasite Plasmodium falciparum.Kanzok SM, Rahlfs S, Becker K, Schirmer RH Methods Enzymol. 2002;347:370-81

44e. Thioredoxin reductase is essential for the survival of Plasmodium falciparum erythrocytic stages.Krnajski Z, Gilberger TW, Walter RD, Cowman AF, Muller S J Biol Chem. 2002 Jul 19;277(29):25970-5;Epub 2002 May 09

44f. Thioredoxin reductase as a pathophysiological factor and drug target.Becker K, Gromer S, Schirmer RH, Muller S Eur J Biochem. 2000 Oct;267(20):6118-25

44g. Redox and antioxidant systems of the malaria parasite Plasmodium falciparum.Muller S Mol Microbiol. 2004 Sep;53(5):1291-305

45a. Gene disruption confirms a critical role for the cysteine protease falcipain-2 in hemoglobin hydrolysis by Plasmodium falciparum.Sijwali PS, Rosenthal PJ Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4384-9

45b. Plasmodium falciparum cysteine protease falcipain-2 cleaves erythrocyte membrane skeletal proteins at late stages of parasite development.Hanspal M, Dua M, Takakuwa Y, Chishti AH, Mizuno A Blood. 2002 Aug 1;100(3):1048-54

45c. Expression and characterization of the Plasmodium falciparum haemoglobinase falcipain-3.Sijwali PS, Shenai BR, Gut J, Singh A, Rosenthal PJ Biochem J. 2001 Dec 1;360(Pt 2):481-9

45d. Characterization of native and recombinant falcipain-2, a principal trophozoite cysteine protease and essential hemoglobinase of Plasmodium falciparum.Shenai BR, Sijwali PS, Singh A, Rosenthal PJ J Biol Chem. 2000 Sep 15;275(37):29000-10

45e. Reducing requirements for hemoglobin hydrolysis by Plasmodium falciparum cysteine proteases.Shenai BR, Rosenthal PJ Mol Biochem Parasitol. 2002 Jun;122(1):99-104

45f. Cysteine proteases of malaria parasites.Rosenthal PJ Int J Parasitol. 2004 Dec;34(13-14):1489-99

45g. Responsiveness of parasite Cys His proteases to iron redox.Lockwood TD Parasitol Res. 2006 Dec;100(1):175-81

45h. Antimalarial activities of novel synthetic cysteine protease inhibitors.Lee BJ, Singh A, Chiang P, Kemp SJ, Goldman EA,Weinhouse MI, Vlasuk GP, Rosenthal PJ Antimicrob Agents Chemother. 2003 Dec;47(12):3810-4

45i. Responsiveness of parasite Cys His proteases to iron redox.Lockwood TD Parasitol Res. 2006 Dec;100(1):175-81

46a. Comparative properties of a three-dimensional model of Plasmodium falciparum ornithine decarboxylase.Birkholtz L, Joubert F, Neitz AW, Louw AI Proteins. 2003 Feb 15;50(3):464-73

46b. The Plasmodium falciparum bifunctional ornithine decarboxylase, S-adenosyl-L-methionine decarboxylase, enables a well balanced polyamine synthesis without domain-domain interaction.Wrenger C, Luersen K, Krause T, Muller S, Walter RD J Biol Chem. 2001 Aug 10;276(32):29651-6

46c. The ornithine decarboxylase domain of the bifunctional ornithine decarboxylase/S-adenosylmethionine decarboxylase of Plasmodium falciparum: recombinant expression and catalytic properties of two different constructs.Krause T, Larsen K, Wrenger C, Gilberger TW, Mauller S,Walter RD Biochem J. 2000 Dec 1;352 Pt 2:287-92

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47a. Plasmodium falciparum: inhibitors of lysosomal cysteine proteinases inhibit a trophozoite proteinase and block parasite development.Rosenthal PJ, McKerrow JH, Rasnick D, Leech JH Mol Biochem Parasitol. 1989 Jun 15;35(2):177-83

47b. Intraerythrocytic Plasmodium falciparum utilizes only a fraction of the amino acids derived from the digestion of host cell cytosol for the biosynthesis of its proteins.Krugliak M, Zhang J, Ginsburg H Mol Biochem Parasitol. 2002 Feb;119(2):249-56

47c. Hemoglobin degradation.Goldberg DE Curr Top Microbiol Immunol. 2005;295:275-91

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47e. Acidification of the malaria parasite’s digestive vacuole by a H+-ATPase and a H+-pyrophosphatase.Saliba KJ, Allen RJ, Zissis S, Bray PG, Ward SA, Kirk K J Biol Chem. 2003 Feb 21;278(8):5605-12

47f. Hemoglobin degradation in Plasmodium-infected red blood cells.Goldberg DE Semin Cell Biol. 1993 Oct;4(5):355-61

47g. Plasmodial hemoglobin degradation:an ordered pathway in a specialized organelle.Goldberg DE Infect Agents Dis. 1992 Aug;1(4):207-11

47h. pH regulation in the intracellular malaria parasite,Plasmodium falciparum. H(+) extrusion via a v-type h(+)-atpase.Saliba KJ, Kirk K J Biol Chem. 1999 Nov 19;274(47):33213-9

48a. Plasmodium falciparum carbohydrate metabolism:a connection between host cell and parasite.Roth E Jr Blood Cells. 1990;16(2-3):453-60; discussion 461-6

48b. The effect of Alcide, a new antimicrobial drug, on rat blood glutathione and erythrocyte osmotic fragility, in vitro.Abdel-Rahman MS, Scatina J J Appl Toxicol. 1985 Jun;5(3):178-81

49a. Development of cysteine protease inhibitors as chemotherapy for parasitic diseases: insights on safety, target validation, and mechanism of action.McKerrow JH Int J Parasitol. 1999 Jun;29(6):833-7

49b. Cysteine proteases of malaria parasites:targets for chemotherapy.Rosenthal PJ, Sijwali PS, Singh A, Shenai BR Curr Pharm Des. 2002;8(18):1659-72

49c. Proteases of malaria parasites:new targets for chemotherapy.Rosenthal PJ Emerg Infect Dis. 1998 Jan-Mar;4(1):49-57

49d. Hydrolysis of erythrocyte proteins by proteases of malaria parasites.Rosenthal PJ Curr Opin Hematol. 2002 Mar;9(2):140-5

49e. Cysteine protease inhibitors as chemotherapy for parasitic infections.McKerrow JH, Engel JC, Caffrey CR Bioorg Med Chem. 1999 Apr;7(4):639-44

50a. In vitro activity of riboflavin against the human malaria parasite Plasmodium falciparum.Akompong T, Ghori N, Haldar K Antimicrob Agents Chemother. 2000 Ja ;44(1):88-96

50b. Potentiation of an antimalarial oxidant drug.Winter RW, Ignatushchenko M, Ogundahunsi OA, Cornell KA,Oduola AM, Hinrichs DJ, Riscoe MK Antimicrob Agents Chemother. 1997 Jul;41(7):1449-54

50c. Hemoglobin metabolism in the malaria parasite Plasmodium falciparum.Francis SE, Sullivan DJ Jr, Goldberg DE Annu Rev Microbiol. 1997;51:97-123

50d. Identification and characterization of heme-interacting proteins in the malaria parasite, Plasmodium falciparum. Campanale N, Nickel C, Daubenberger CA, Wehlan DA,Gorman JJ, Klonis N, Becker K, Tilley L J Biol Chem. 2003 Jul 25;278(30):27354-61

50e. The redox status of malaria-infected erythrocytes:an overview with an emphasis on unresolved problems.Ginsburg H, Atamna H Parasite. 1994 Mar;1(1):5-13

50f. Redox and antioxidant systems of the malaria parasite Plasmodium falciparum.Muller S Mol Microbiol. 2004 Sep;53(5):1291-305

50g. Origin of reactive oxygen species in erythrocytes infected with Plasmodium falciparum.Atamna H, Ginsburg H Mol Biochem Parasitol. 1993 Oct;61(2):231-41 Erratum in: Mol Biochem Parasitol 1994 Feb;63(2):312

50h. Oxidative stress in malaria parasite-infected erythrocytes: host-parasite interactions.Becker K, Tilley L, Vennerstrom JL, Roberts D,Rogerson S, Ginsburg H Int J Parasitol. 2004 Feb;34(2):163-89

50i. Clotrimazole binds to heme and enhances heme-dependent hemolysis: proposed antimalarial mechanism of clotrimazole.Huy NT, Kamei K, Yamamoto T, Kondo Y, Kanaori K,Takano R, Tajima K, Hara S J Biol Chem. 2002 Feb 8;277(6):4152-8

50j. Illumination of the malaria parasite Plasmodium falciparum alters intracellular pH. Implications for live cell imaging.Wissing F, Sanchez CP, Rohrbach P, Ricken S, Lanzer M J Biol Chem. 2002 Oct 4;277(40):37747-55

50k. Potentiation of an antimalarial oxidant drug.Winter RW, Ignatushchenko M, Ogundahunsi OA, Cornell KA,Oduola AM, Hinrichs DJ, Riscoe MK Antimicrob Agents Chemother. 1997 Jul;41(7):1449-54

50L. The iron environment in heme and heme-antimalarial complexes of pharmacological interest. Adams PA, Berman PA, Egan TJ, Marsh PJ, Silver J J Inorg Biochem. 1996 Jul;63(1):69-77

50m. Lysis of malarial parasites and erythrocytes by ferriprotoporphyrin IX-chloroquine and the inhibition of this effect by proteins.Zhang Y, Hempelmann E Biochem Pharmacol. 1987 Apr 15;36(8):1267-73

50n. Ferriprotoporphyrin IX: a mediator of the antimalarial action of oxidants and 4-aminoquinoline drugs.Fitch CD, Dutta P, Kanjananggulpan P, Chevli R Prog Clin Biol Res. 1984;155:119-30

50o. Hemolysis of mouse erythrocytes by ferriprotoporphyrin IX and chloroquine. Chemotherapeutic implications.Chou AC, Fitch CD J Clin Invest. 1980 Oct;66(4):856-8

50p. Is hemin responsible for the susceptibility of Plasmodia to oxidant stress?Har-El R, Marva E, Chevion M, Golenser JFree Radic Res Commun. 1993;18(5):279-90

50q. The effects of ascorbate-induced free radicals on Plasmodium falciparum.Marva E, Golenser J, Cohen A, Kitrossky N, Har-el R,Chevion M Trop Med Parasitol. 1992 Mar;43(1):17-23

50r. Induction of oxidant stress by iron available in advanced forms of Plasmodium falciparum.Golenser J, Marva E, Har-El R, Chevion M Free Radic Res Commun. 1991;12-13 Pt 2:639-43

50s. Growth inhibition of Plasmodium falciparum involving carbon centered iron-chelate radical (L., X-)-Fe(III)based on pyridoxal-betaine. A novel type of antimalarials active against chloroquine-resistant parasites.Iheanacho EN, Sarel S, Samuni A, Avramovici-Grisaru S,Spira DT Free Radic Res Commun. 1991;15(1):1-10

50t. Detection of short-chain carbonyl products of lipid peroxidation from malaria-parasite (Plasmodium vinckei)-infected red blood cells exposed to oxidative stress.Buffinton GD, Hunt NH, Cowden WB, Clark IA Biochem J. 1988 Jan 1;249(1):63-8

50u. Ferriprotoporphyrin IX: a mediator of the antimalarial action of oxidants and 4-aminoquinoline drugs.Fitch CD, Dutta P, Kanjananggulpan P, Chevli R Prog Clin Biol Res. 1984;155:119-30

50v. Influence of chloroquine treatment and Plasmodium falciparum malaria infection on some enzymatic and non-enzymatic antioxidant defense indices in humans.Farombi EO, Shyntum YY, Emerole GO Drug Chem Toxicol. 2003 Feb;26(1):59-71

50w. Oxidative stress in patients with non-complicated malaria.Paban A, Carmona J, Burgos LC, Blair S Clin Biochem. 2003 Feb;36(1):71-8

50x. Evidence for erythrocyte lipid peroxidation in acute falciparum malaria.Das BS, Nanda NK Trans R Soc Trop Med Hyg. 1999 Jan-Feb;93(1):58-62

50y. Metal chelators/antioxidants: approaches to protect erythrocytic oxidative stress injury during Plasmodium berghei infection in Mastomys coucha.Srivastava PJ, Chandra S, Arif AJ, Singh C, Panday V Pharmacol Res. 1999 Sep;40(3):239-41

50z. Role of free radicals in Plasmodium berghei infected Mastomys natalensis brain.Mahdi AA, Chander R, Kapoor NK, Ahmad S Indian J Exp Biol. 1992 Dec;30(12):1193-6

50aa. Plasmodium falciparum induced perturbations of the erythrocyte antioxidant system.Mohan K, Dubey ML, Ganguly NK, Mahajan RC Clin Chim Acta. 1992 Jul 31;209(1-2):19-26

50bb. Effect of radical treatment on erythrocyte lipid peroxidation in Plasmodium vivax-infected malaria patients.Mathews ST, Selvam R Biochem Int. 1991 Sep;25(2):211-20

51a. The survival of Plasmodium Under oxidant stress.Golenser J, Marva E, Chevion M Parasitol Today. 1991 Jun;7(6):142-6

51b. Hexose-monophosphate shunt activity in intact Plasmodium falciparum-infected erythrocytes and in free parasites.Atamna H, Pascarmona G, Ginsburg H Mol Biochem Parasitol. 1994 Sep;67(1):79-89

51c. Vampires, Pasteur and reactive oxygen species.Is the switch from aerobic to anaerobic metabolism a preventive antioxidant defence in blood-feeding parasites?Oliveira PL, Oliveira MF FEBS Lett. 2002 Aug 14;525(1-3):3-6

51d. Oxidative stress and malaria-infected erythrocytes.Mishra NC, Kabilan L, Sharma A Indian J Malariol. 1994 Jun;31(2):77-87

51e. Oxidative stress and antioxidant defence mechanism in Plasmodium vivax malaria before and after chloroquine treatment.Sarin K, Kumar A, Prakash A, Sharma A Indian J Malariol. 1993 Sep;30(3):127-33

51f. Lipid peroxidation in Plasmodium falciparum-parasitized human erythrocytes.Simões AP, van den Berg JJ, Roelofsen B, Op den Kamp JA Arch Biochem Biophys. 1992 Nov 1;298(2):651-7

51g. The adaptation of Plasmodium falciparum to oxidative stress in G6PD deficient human erythrocytes.Roth E Jr, Schulman S Br J Haematol. 1988 Nov;70(3):363-7

51h. Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte:can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?Roth EF Jr, Schulman S, Vanderberg J, Olson J Blood. 1986 Mar;67(3):827-30

51i. The plasmodial apicoplast was retained under evolutionary selective pressure to assuage blood stage oxidative stress. Toler S Med Hypotheses. 2005;65(4):683-90

51j. Glutathione–functions and metabolism in the malarial parasite Plasmodium falciparum.Becker K, Rahlfs S, Nickel C, Schirmer RH Biol Chem. 2003 Apr;384(4):551-66

51k. Oxidative stress and antioxidant defenses:a target for the treatment of diseases caused by parasitic protozoa.Turrens JF Mol Aspects Med. 2004 Feb-Apr;25(1-2):211-20

51L. Vampires, Pasteur and reactive oxygen species.Is the switch from aerobic to anaerobic metabolism a preventive antioxidant defence in blood-feeding parasites?Oliveira PL, Oliveira MF FEBS Lett. 2002 Aug 14;525(1-3):3-6

51m. The malaria parasite supplies glutathione to its host cell–investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum.Atamna H, Ginsburg H Eur J Biochem. 1997 Dec 15;250(3):670-9

51n. Redox processes in malaria and other parasitic diseases.Determination of intracellular glutathione.Becker K, Gui M, Traxler A, Kirsten C, Schirmer RH Histochemistry. 1994 Nov;102(5):389-95

52a. Effect of antifungal azoles on the heme detoxification system of malarial parasite.Huy NT, Kamei K, Kondo Y, Serada S, Kanaori K, Takano R,Tajima K, Hara S J Biochem (Tokyo). 2002 Mar;131(3):437-44

52b. Malarial haemozoin/beta-haematin supports haempolymerization in the absence of protein.Dorn A, Stoffel R, Matile H, Bubendorf A, Ridley RG Nature. 1995 Mar 16;374(6519):269-71

52c. Plasmodium falciparum histidine-rich protein-2 (PfHRP2) modulates the redox activity of ferri-protoporphyrin IX (FePPIX): peroxidase-like activity of the PfHRP2-FePPIX complex.Mashima R, Tilley L, Siomos MA, Papalexis V,Raftery MJ, Stocker R J Biol Chem. 2002 Apr 26;277(17):14514-20

52d. Hemoglobin degradation in malaria-infected erythrocytes determined from live cell magnetophoresis.Moore LR, Fujioka H, Williams PS, Chalmers JJ, Grimberg B,Zimmerman PA, Zborowski M FASEB J. 2006 Apr;20(6):747-9

52e. A physiochemical mechanism of hemozoin (beta-hematin)synthesis by malaria parasite.Tripathi AK, Garg SK, Tekwani BL Biochem Biophys Res Commun. 2002 Jan 11;290(1):595-601

52f. Histidine-rich protein 2 of the malaria parasite,Plasmodium falciparum, is involved in detoxification of the by-products of haemoglobin degradation.Papalexis V, Siomos MA, Campanale N, Guo X, Kocak G,Foley M, Tilley L Mol Biochem Parasitol. 2001 Jun;115(1):77-86

52g. Theories on malarial pigment formation and quinoline action.Sullivan DJ Int J Parasitol. 2002 Dec 4;32(13):1645-53

52h. A comparison and analysis of several ways to promote haematin (haem) polymerisation and an assessment of its initiation in vitro.Dorn A, Vippagunta SR, Matile H, Bubendorf A,Vennerstrom JL, Ridley RG Biochem Pharmacol. 1998 Mar 15;55(6):737-47

52i. Plasmodium hemozoin formation mediated by histidine-rich proteins.Sullivan DJ Jr, Gluzman IY, Goldberg DE Science. 1996 Jan 12;271(5246):219-22

52j. An iron-carboxylate bond links the heme units of malaria pigment.Slater AF, Swiggard WJ, Orton BR, Flitter WD, Goldberg DE, Cerami A, Henderson GB Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):325-9

52k. Hemozoin induces macrophage chemokine expression through oxidative stress-dependent and -independent mechanisms.Jaramillo M, Godbout M, Olivier M J Immunol. 2005 Jan 1;174(1):475-84

53a. A non-radiolabeled heme-GSH interaction test for the screening of antimalarial compounds.Garavito G, Monje MC, Maurel S, Valentin A, Nepveu F,Deharo E Exp Parasitol. 2007 Jan 23

53b. Effect of antifungal azoles on the heme detoxification system of malarial parasite.Huy NT, Kamei K, Kondo Y, Serada S, Kanaori K, Takano R,Tajima K, Hara S J Biochem (Tokyo). 2002 Mar;131(3):437-44

54a. A comparison of the effects of ocular preservatives on mammalian and microbial ATP and glutathione levels.Ingram PR, Pitt AR, Wilson CG, Olejnik O, Spickett CM Free Radic Res. 2004 Jul;38(7):739-50

54b. The effect of Alcide, a new antimicrobial drug,on rat blood glutathione and erythrocyte osmotic fragility, in vitro.Abdel-Rahman MS, Scatina J, Appl Toxicol. 1985 Jun;5(3):178-81

55a. Inhibition of the peroxidative degradation of haem as the basis of action of chloroquine and other quinoline antimalarials.Loria P, Miller S, Foley M, Tilley L Biochem J. 1999 Apr 15;339 ( Pt 2):363-70

55b. Quinoline antimalarials: mechanisms of action and resistance and prospects for new agents.Foley M, Tilley L Pharmacol Ther. 1998 Jul;79(1):55-87

55c. Quinoline antimalarials:mechanisms of action and resistance.Foley M, illey L Int J Parasitol. 1997 Feb;27(2):231-40

55d. Inhibition by anti-malarial drugs of haemoglobin denaturation and iron release in acidified red blood cell lysates–a possible mechanism of their anti-malarial effect?Gabay T, Krugliak M, Shalmiev G, Ginsburg H Parasitology. 1994 May;108 ( Pt 4):371-81

55e. Chloroquine: mechanism of drug action and resistance in Plasmodium falciparum.Slater AF Pharmacol Ther. 1993 Feb-Mar;57(2-3):203-35

55f. The treatment of Plasmodium falciparum-infected erythrocytes with chloroquine leads to accumulation of ferriprotoporphyrin IX bound to particular parasite proteins and to the inhibition of the parasite’s 6-phosphogluconate dehydrogenase.Famin O, Ginsburg H Parasite. 2003 Mar;10(1):39-50

55g. Chloroquine – some open questions on its antimalarial mode of action and resistance.Ginsburg H, Krugliak M Drug Resist Updat. 1999 Jun;2(3):180-187

55h. Kinetics of inhibition of glutathione-mediated degradation of ferriprotoporphyrin IX by antimalarial drugs.Famin O, Krugliak M, Ginsburg H Biochem Pharmacol. 1999 Jul 1;58(1):59-68

55i. The fate of ferriprotorphyrin IX in malaria infected erythrocytes in conjunction with the mode of action of antimalarial drugs.Zhang J, Krugliak M, Ginsburg H Mol Biochem Parasitol. 1999 Mar 15;99(1):129-41

55j. Inhibition of glutathione-dependent degradation of heme by chloroquine and amodiaquine as a possible basis for their antimalarial mode of action.Ginsburg H, Famin O, Zhang J, Krugliak M Biochem Pharmacol. 1998 Nov 15;56(10):1305-13

55k. Antimalarial drugs inhibiting hemozoin (beta-hematin)formation: a mechanistic update.Kumar S, Guha M, Choubey V, Maity P, Bandyopadhyay U Life Sci. 2007 Feb 6;80(9):813-28

55L. A medicinal chemistry perspective on 4-aminoquinoline antimalarial drugs.O’Neill PM, Ward SA, Berry NG, Jeyadevan JP, Biagini GA,Asadollaly E, Park BK, Bray PG Curr Top Med Chem. 2006;6(5):479-507

55m. Heme Aggregation inhibitors: antimalarial drugs targeting an essential biomineralization process.Ziegler J, Linck R, Wright DW Curr Med Chem. 2001 Feb;8(2):171-89

55n. Structural specificity of chloroquine-hematin binding related to inhibition of hematin polymerization and parasite growth.Vippagunta SR, Dorn A, Matile H, Bhattacharjee AK,Karle JM, Ellis WY, Ridley RG, Vennerstrom JL J Med Chem. 1999 Nov 4;42(22):4630-9

55o. A common mechanism for blockade of heme polymerization by antimalarial quinolines.Sullivan DJ Jr, Matile H, Ridley RG, Goldberg DE J Biol Chem. 1998 Nov 20;273(47):31103-7

55p. Central role of hemoglobin degradation in mechanisms of action of 4-aminoquinolines, quinoline methanols,and phenanthrene methanols.Mungthin M, Bray PG, Ridley RG, Ward SA Antimicrob Agents Chemother. 1998 Nov;42(11):2973-

55q. Access to hematin: the basis of chloroquine resistance.Bray PG, Mungthin M, Ridley RG, Ward SA

55r. Involvement of heme in the antimalarial action of chloroquine.Fitch CD Trans Am Clin Climatol Assoc. 1998;109:97-105; discussion 105-6

55s. Relationship between antimalarial drug activity,accumulation, and inhibition of heme polymerization in Plasmodium falciparum in vitro.Hawley SR, Bray PG, Mungthin M, Atkinson JD, O’Neill PM,Ward SA Antimicrob Agents Chemother. 1998 Mar;42(3):682-6

55t. Haematin (haem) polymerization and its inhibition by quinoline antimalarials.Ridley RG, Dorn A, Vippagunta SR, Vennerstrom JL Ann Trop Med Parasitol. 1997 Jul;91(5):559-66

55u. Heme polymerase activity and the stage specificity of antimalarial action of chloroquine.Orjih AU J Pharmacol Exp Ther. 1997 Jul;282(1):108-12

55v. Xanthones as antimalarial agents;studies of a possible mode of action.Ignatushchenko MV, Winter RW, Bächinger HP, Hinrichs DJ,Riscoe MK FEBS Lett. 1997 Jun 2;409(1):67-73

55w. Depolymerization of malarial hemozoin: a novel reaction initiated by blood schizontocidal antimalarials.Pandey AV, Tekwani BL FEBS Lett. 1997 Feb 3;402(2-3):236-40

55x. On the molecular mechanism of chloroquine’s antimalarial action.Sullivan DJ Jr, Gluzman IY, Russell DG, Goldberg DE Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11865-70

55y. Hemoglobin catabolism and the killing of intraerythrocytic Plasmodium falciparum by chloroquine.Orjih AU, Ryerse JS, Fitch CD Experientia. 1994 Jan 15;50(1):34-9

55z. Antimalarial 4-aminoquinolines: mode of action and pharmacokinetics.Pussard E, Verdier F Fundam Clin Pharmacol. 1994;8(1):1-17

55aa. Hemoglobin catabolism and host-parasite heme balance in chloroquine-sensitive and chloroquine-resistant Plasmodium berghei infections.Wood PA, Eaton JW Am J Trop Med Hyg. 1993 Apr;48(4):465-72

55bb. Quinoline-containing antimalarials–mode of action, drug resistance and its reversal.An update with unresolved puzzles.Ginsburg H, Krugliak M Biochem Pharmacol. 1992 Jan 9;43(1):63-70

55cc. Inhibition by chloroquine of a novel haempolymerase enzyme activity in malaria trophozoites.Slater AF, Cerami A Nature. 1992 Jan 9;355(6356):167-9 Comment in: Nature. 1992 Jan 9;355(6356):108-9

55dd. Heme polymerase: modulation by chloroquine treatment of a rodent malaria.Chou AC, Fitch CD Life Sci. 1992;51(26):2073-8

55ee. Mode of action of antimalarial drugs.Fitch CD Ciba Found Symp. 1983;94:222-32

55ff. Binding of antimalarial drugs to hemozoin from Plasmodium berghei.Jearnpipatkul A, Govitrapong P, Yuthavong Y, Wilairat P,Panijpan B Experientia. 1980 Sep 15;36(9):1063-4

55gg. Influence of chloroquine treatment and Plasmodium falciparum malaria infection on some enzymatic and non-enzymatic antioxidant defense indices in humans.Farombi EO, Shyntum YY, Emerole GO Drug Chem Toxicol. 2003 Feb;26(1):59-71

56a. Regulation of intracellular glutathione levels in erythrocytes infected with chloroquine-sensitive and chloroquine-resistant Plasmodium falciparum.Meierjohann S, Walter RD, Muller S, Müller S Biochem J. 2002 Dec 15;368(Pt 3):761-8

56b. The malaria parasite supplies glutathione to its host cell–investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum.Atamna H, Ginsburg H Eur J Biochem. 1997 Dec 15;250(3):670-9

56c. Is the expression of genes encoding enzymes of glutathione (GSH) metabolism involved in chloroquine resistance in Plasmodium chabaudi parasites?Ferreira ID, Nogueira F, Borges ST, do Rosario VE,Cravo P, do Rosyo VE Mol Biochem Parasitol. 2004 Jul;136(1):43-50

56d. Plasmodium falciparum glutathione metabolism and growth are independent of glutathione system of host erythrocyte.Ayi K, Cappadoro M, Branca M, Turrini F, Arese P FEBS Lett. 1998 Mar 13;424(3):257-61

56e. Glutathione-S-transferases from chloroquine-resistant and -sensitive strains of Plasmodium falciparum:what are their differences?Rojpibulstit P, Kangsadalampai S, Ratanavalachai T,Denduangboripant J, Chavalitshewinkoon-Petmitr P Southeast Asian J Trop Med Public Health. 2004 Jun;35(2):292-9

56f. Plasmodium berghei: analysis of the gamma-glutamylcysteine synthetase gene in drug-resistant lines.Perez-Rosado J, Gervais GW, Ferrer-Rodriguez I, Peters W,Serrano AE, Pérez-Rosado J, Ferrer-RodrÃguez I Exp Parasitol. 2002 Aug;101(4):175-82

56g. Glutathione-S-transferase activity in malarial parasites.Srivastava P, Puri SK, Kamboj KK, Pandey VC Trop Med Int Health. 1999 Apr;4(4):251-4

56h. Role of glutathione in the detoxification of ferriprotoporphyrin IX in chloroquine resistant Plasmodium berghei.Platel DF, Mangou F, Tribouley-Duret J Mol Biochem Parasitol. 1999 Jan 25;98(2):215-23

56i. Plasmodium berghei: implication of intracellular glutathione and its related enzyme in chloroquine resistance in vivo.Dubois VL, Platel DF, Pauly G, Tribouley-Duret J Exp Parasitol. 1995 Aug;81(1):117-24

56j. Amodiaquine failure associated with erythrocytic glutathione in Plasmodium falciparum malaria.Zuluaga L, Pabon A, Lopez C, Ochoa A, Blair S Malar J. 2007 Apr 23;6(1):47

57a. A prodrug form of a Plasmodium falciparum glutathione reductase inhibitor conjugated with a 4-anilinoquinoline.Davioud-Charvet E, Delarue S, Biot C, Schwobel B, Boehme CC,Mussigbrodt A, Maes L, Sergheraert C,Grellier P,Schirmer RH, Becker K, Schwarbel B, Maussigbrodt A J Med Chem. 2001 Nov 22;44(24):4268-76

57b. Deletion of the parasite-specific insertions and mutation of the catalytic triad in glutathione reductase from chloroquine-sensitive Plasmodium falciparum 3D7.Gilberger TW, Schirmer RH, Walter RD, Mauller S Mol Biochem Parasitol. 2000 Apr 15;107(2):169-79

57c. Potentiation of the antimalarial action of chloroquine in rodent malaria by drugs known to reduce cellular glutathione levels.Deharo E, Barkan D, Krugliak M, Golenser J, Ginsburg H Biochem Pharmacol. 2003 Sep 1;66(5):809-17

57d. Glutathione is involved in the antimalarial action of chloroquine and its modulation affects drug sensitivity of human and murine species of Plasmodium.Ginsburg H, Golenser J Redox Rep. 2003;8(5):276-9

57e. Double-drug development against antioxidant enzymes from Plasmodium falciparum.Biot C, Dessolin J, Grellier P, Davioud-Charvet E Redox Rep. 2003;8(5):280-3

57f. Plasmodium falciparum: in vitro interactions of artemisinin with amodiaquine, pyronaridine,and chloroquine Gupta S, Thapar MM, Mariga ST, Wernsdorfer WH, Bjorkman A Exp Parasitol. 2002 Jan;100(1):28-35

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58a. Oxidation of pharmaceuticals during water treatment with chlorine dioxide.Huber MM, Korhonen S, Ternes TA, von Gunten U Water Res. 2005 Sep;39(15):3607-17

59a. Malarial parasite hexokinase and hexokinase-dependent glutathione reduction in the Plasmodium falciparum infected human erythrocyte.Roth EF Jr J Biol Chem. 1987 Nov 15;262(32):15678-82

59b. Double-drug development against antioxidant enzymes from Plasmodium falciparum.Biot C, Dessolin J, Grellier P,Davioud-Charvet E Redox Rep. 2003;8(5):280-3

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59d. Hexose-monophosphate shunt activity in intact Plasmodium falciparum-infected erythrocytes andin free parasites.Atamna H, Pascarmona G, Ginsburg H Mol Biochem Parasitol. 1994 Sep;67(1):79-89

60a. Redox metabolism in glucose-6-phosphate dehydrogenase deficient erythrocytes and its relation to antimalarial chemotherapy.Ginsburg H, Golenser J Parassitologia. 1999 Sep;41(1-3):309-11

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60c. Plasmodium berghei: dehydroepiandrosterone sulfate reverses chloroquino-resistance in experimental malaria infection; correlation with glucose 6-phosphate dehydrogenase and glutathione synthesis pathway.Safeukui I, Mangou F, Malvy D, Vincendeau P,Mossalayi D, Haumont G, Vatan R, Olliaro P, Millet P Biochem Pharmacol. 2004 Nov 15;68(10):1903-10

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60f. Ribose metabolism and nucleic acid synthesis in normal and glucose-6-phosphate dehydrogenase-deficient human erythrocytes infected with Plasmodium falciparum.Roth EF Jr, Ruprecht RM, Schulman S, Vanderberg J, Olson JA J Clin Invest. 1986 Apr;77(4):1129-35

60g. The effect of X chromosome inactivation on the inhibition of Plasmodium falciparum malaria growth by glucose-6-phosphate-dehydrogenase-deficient red cells.Roth EF Jr, Raventos Suarez C, Rinaldi A, Nagel RL Blood. 1983 Oct;62(4):866-8

60h. Excess release of ferriheme in G6PD-deficient erythrocytes: possible cause of hemolysis and resistance to malaria.Janney SK, Joist JJ, Fitch CD Blood. 1986 Feb;67(2):331-3

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62b. Removal of chlorine dioxide disinfection by-products by ferrous salts.Katz A, Narkis N Water Res. 2001 Jan;35(1):101-8

62c. Chlorine dioxide reduction by aqueous iron(II) through outer-sphere and inner-sphere electron-transfer pathways.Wang L, Odeh IN, Margerum DW Inorg Chem. 2004 Nov 15;43(23):7545-51

62d. Electrochemical metalloporphyrin-catalyzed reduction of chlorite.Collman JP, Boulatov R, Sunderland CJ, Shiryaeva IM,Berg KE J Am Chem Soc. 2002 Sep 11;124(36):10670-1

63a. Potency ranking of methemoglobin-forming agents.French CL, Yaun SS, Baldwin LA, Leonard DA, Zhao XQ,Calabrese EJ J Appl Toxicol. 1995 May-Jun;15(3):167-74

63b. Theoretical mechanistic basis of oxidants of methaemoglobin formation.Akintonwa DA Med Hypotheses. 2000 Feb;54(2):312-20

64a. Design, synthesis and antimalarial activity of a new class of iron chelators.Solomon VR, Haq W, Puri SK, Srivastava K, Katti SB Med Chem. 2006 Mar;2(2):133-8

64b. Heme biosynthesis by the malarial parasite.Import of delta-aminolevulinate dehydrase from the host red cell.Bonday ZQ, Taketani S, Gupta PD, Padmanaban G J Biol Chem. 1997 Aug 29;272(35):21839-46

64c. Hemoglobin catabolism and iron utilization by malaria parasites.Rosenthal PJ, Meshnick SR Mol Biochem Parasitol. 1996 Dec 20;83(2):131-9

64d. Heme metabolism of Plasmodium is a major antimalarial target.Padmanaban G, Rangarajan PN Biochem Biophys Res Commun. 2000 Feb 24;268(3):665-8

64e. Iron chelators: mode of action as antimalarials.Cabantchik ZI, Glickstein H, Golenser J, Loyevsky M,Tsafack A Acta Haematol. 1996;95(1):70-7

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65a. The plant-type ferredoxin-NADP+ reductase/ferredoxin redox system as a possible drug target against apicomplexan human parasites.Seeber F, Aliverti A, Zanetti G Curr Pharm Des. 2005;11(24):3159-72

65b. Ferredoxin-NADP(+) Reductase from Plasmodium falciparum Undergoes NADP(+)-dependent Dimerization and Inactivation:Functional and Crystallographic Analysis.Milani M, Balconi E, Aliverti A, Mastrangelo E, Seeber F,Bolognesi M, Zanetti G J Mol Biol. 2007 Mar 23;367(2):501-13

65c. Cloning and Characterization of Ferredoxin and Ferredoxin-NADP+ Reductase from Human Malaria Parasite.Kimata-Ariga Y, Kurisu G, Kusunoki M, Aoki S, Sato D,Kobayashi T, Kita K, Horii T, Hase TJ Biochem (Tokyo). 2007 Mar;141(3):421-428;Epub 2007 Jan 23

65d. Reconstitution of an apicoplast-localised electron transfer pathway involved in the isoprenoid Röhrich RC, Englert N, Troschke K, Reichenberg A, Hintz M,Seeber F, Balconi E, Aliverti A, Zanetti G, Köhler U,Pfeiffer M, Beck E, Jomaa H, Wiesner J FEBS Lett. 2005 Nov 21;579(28):6433-8;Epub 2005 Nov 02

65e. The plant-type ferredoxin-NADP+ reductase/ferredoxin redox system as a possible drug target against apicomplexan human parasites.Seeber F, Aliverti A, Zanetti G Curr Pharm Des. 2005;11(24):3159-72

65f. Biogenesis of iron-sulphur clusters in amitochondriate and apicomplexan protists. Seeber FInt J Parasitol. 2002 Sep;32(10):1207-17

65g. Apicomplexan parasites possess distinct nuclear-encoded,but apicoplast-localized, plant-type ferredoxin-NADP+reductase and ferredoxin.Vollmer M, Thomsen N, Wiek S, Seeber F J Biol Chem. 2001 Feb 23;276(8):5483-90;Epub 2000 Oct 30

66a. Superoxide dismutase as a target enzyme for Fe-porphyrin-induced cell death.Asayama S, Kasugai N, Kubota S, Nagaoka S, Kawakami H J Inorg Biochem. 2007 Feb;101(2):261-6

66b. The crystal structure of superoxide dismutase from Plasmodium falciparum.Boucher IW, Brzozowski AM, Brannigan JA, Schnick C,Smith DJ, Kyes SA, Wilkinson AJ BMC Struct Biol. 2006;6:20

66c. Identification of a mitochondrial superoxide dismutase with an unusual targeting sequence in Plasmodium falciparum.Sienkiewicz N, Daher W, Dive D, Wrenger C, Viscogliosi E,Wintjens R, Jouin H, Capron M, Mauller S, Khalife JMol Biochem Parasitol. 2004 Sep;137(1):121-32

66d. Oxidative stress and antioxidant defenses:a target for the treatment of diseases caused by parasitic protozoa.Turrens JFMol Aspects Med. 2004 Feb-Apr;25(1-2):211-20

66e. Screening of Plasmodium falciparum iron superoxide dismutase inhibitors and accuracy of the SOD-assays.Soulare L, Delplace P, Davioud-Charvet E, Py S,Sergheraert C, Ricard I, Hoffmann P, Dive D Bioorg Med Chem. 2003 Nov 17;11(23):4941-4

66f. Superoxide dismutase in Plasmodium: a current survey.Dive D, Gratepanche S, Yera H, Baccuwe P, Daher W,Delplace P, Odberg-Ferragut C, Capron M, Khalife J Redox Rep. 2003;8(5):265-7

66g. Biochemical and electron paramagnetic resonance study of the iron superoxide dismutase from Plasmodium falciparum.Gratepanche S, Macnage S, Touati D, Wintjens R, Delplace P,Fontecave M, Masset A, Camus D, Dive D Mol Biochem Parasitol. 2002 Apr 9;120(2):237-46

66h. Cloning and characterization of iron-containing superoxide dismutase from the human malaria species Plasmodium ovale, P. malariae and P. vivax.Baert CB, Deloron P, Viscogliosi E, Delgado-Viscogliosi P,Camus D, Dive D Parasitol Res. 1999 Dec;85(12):1018-24

66i. The role of superoxide dismutation in malaria parasites.Schwartz E, Samuni A, Friedman I, Hempelmann E, Golenser J Inflammation. 1999 Aug;23(4):361-70

66j. Characterization of iron-dependent endogenous superoxide dismutase of Plasmodium falciparum.Baccuwe P,Gratepanche S, Fourmaux MN, Van Beeumen J,Samyn B, Mercereau-Puijalon O, Touzel JP, Slomianny C,Camus D, Dive D Mol Biochem Parasitol. 1996 Feb-Mar;76(1-2):125-34

66k. Subcellular distribution of superoxide dismutase and catalase in human malarial parasite Plasmodium vivax.Sharma A Indian J Exp Biol. 1993 Mar;31(3):275-7

66L. Presence of an endogenous superoxide dismutase activity in three rodent malaria species.Baccuwe P, Slomianny C, Camus D, Dive D Parasitol Res. 1993;79(5):349-52

66m. Oxidant defense enzymes of Plasmodium falciparum.Fairfield AS, Abosch A, Ranz A, Eaton JW, Meshnick SR Mol Biochem Parasitol. 1988 Jul;30(1):77-82

67a. Structural metal dependency of the arginase from the human malaria parasite Plasmodium falciparum.Mauller IB, Walter RD, Wrenger C Biol Chem. 2005 Feb;386(2):117-26

68a. Targeting enzymes involved in spermidine metabolism of parasitic protozoa–a possible new strategy for anti-parasitic treatment.Kaiser A, Gottwald A, Maier W, Seitz HM Parasitol Res. 2003 Dec;91(6):508-16

68b. Cellular polyamine profile of the phyla Dinophyta,Apicomplexa, Ciliophora, Euglenozoa, Cercozoa and Heterokonta.Hamana K, Sakamoto A, Nishina M, Niitsu M J Gen Appl Microbiol. 2004 Oct;50(5):297-303

68c. Diamine derivatives with antiparasitic activities.Labadie GR, Choi SR, Avery MA Bioorg Med Chem Lett. 2004 Feb 9;14(3):615-9

68d. Spermidine metabolism in parasitic protozoa–a comparison to the situation in prokaryotes, viruses,plants and fungi.Kaiser AE, Gottwald AM, Wiersch CS, Maier WA, Seitz HM Folia Parasitol (Praha). 2003 Mar;50(1):3-18

69a. Polyamines in the cell cycle of the malarial parasite Plasmodium falciparum.Bachrach U, Abu-Elheiga L, Assaraf YG, Golenser J, Spira DT Adv Exp Med Biol. 1988;250:643-50

69b. Polyamine synthesis and salvage pathways in the malaria parasite Plasmodium falciparum.Ramya TN, Surolia N, Surolia A Biochem Biophys Res Commun. 2006 Sep 22;348(2):579-84

69c. The spermidine synthase of the malaria parasite Plasmodium falciparum: molecular and biochemical characterisation of the polyamine synthesis enzyme.Haider N, Eschbach ML, Dias Sde S, Gilberger TW, Walter RD,Larsen K Mol Biochem Parasitol. 2005 Aug;142(2):224-36

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69e. The Plasmodium falciparum bifunctional ornithine decarboxylase, S-adenosyl-L-methionine decarboxylase,enables a well balanced polyamine synthesis without domain-domain interaction.Wrenger C, Luersen K, Krause T, Muller S, Walter RD J Biol Chem. 2001 Aug 10;276(32):29651-6

69f. Effect of polyamines on the activity of malarial alpha-like DNA polymerase.Bachrach U, Abu-Elheiga L Eur J Biochem. 1990 Aug 17;191(3):633-7

69g. Plasmodium falciparum: purification, properties,and immunochemical study of ornithine decarboxylase,the key enzyme in polyamine biosynthesis.Assaraf YG, Kahana C, Spira DT, Bachrach U Exp Parasitol. 1988 Oct;67(1):20-30

69h. Polyamines in the cell cycle of the malarial parasite Plasmodium falciparum.Bachrach U, Abu-Elheiga L, Assaraf YG, Golenser J,Spira DT Adv Exp Med Biol. 1988;250:643-50

69i. Effect of polyamine depletion on macromolecular synthesis of the malarial parasite, Plasmodium falciparum, cultured in human erythrocytes.Assaraf YG, Abu-Elheiga L, Spira DT, Desser H, Bachrach U Biochem J. 1987 Feb 15;242(1):221-6

69j. Polyamine levels and the activity of their biosynthetic enzymes in human erythrocytes infected with the malarial parasite, Plasmodium falciparum.Assaraf YG, Golenser J, Spira DT, Bachrach U Biochem J. 1984 Sep 15;222(3):815-9

69k. Plasmodium berghei: inhibitors of ornithine decarboxylase block exoerythrocytic schizogony.Hollingdale MR, McCann PP, Sjoerdsma A Exp Parasitol. 1985 Aug;60(1):111-7

70a. 3-Aminooxy-1-aminopropane and derivatives have an antiproliferative effect on cultured Plasmodium falciparum by decreasing intracellular polyamine concentrations.Das Gupta R, Krause-Ihle T, Bergmann B, Mauller IB,Khomutov AR, Mauller S, Walter RD, Larsen K Antimicrob Agents Chemother. 2005 Jul;49(7):2857-64

70b. Antimalarial effect of agmatine on Plasmodium berghei K173 strain.Su RB, Wei XL, Liu Y, Li J Acta Pharmacol Sin. 2003 Sep;24(9):918-22

70c. Antiplasmodial activity of a series of 1,3,5-triazine-substituted polyamines.Klenke B, Barrett MP, Brun R, Gilbert IH J Antimicrob Chemother. 2003 Aug;52(2):290-3

70d. Effect of drugs inhibiting spermidine biosynthesis and metabolism on the in vitro development of Plasmodium falciparum.Kaiser A, Gottwald A, Wiersch C, Lindenthal B, Maier W,Seitz HM Parasitol Res. 2001 Nov;87(11):963-72

70e. Polyamine metabolism in various tissues during pathogenesis of chloroquine-susceptible and resistant malaria.Mishra M, Chandra S, Pandey VC, Tekwani BL Cell Biochem Funct. 1997 Dec;15(4):229-35

70f. Combined action of inhibitors of S-adenosylmethionine decarboxylase with an antimalarial drug, chloroquine,on Plasmodium falciparum.Das B, Gupta R, Madhubala R J Eukaryot Microbiol. 1997 Jan-Feb;44(1):12-7

70g. Combined action of inhibitors of polyamine biosynthetic pathway with a known antimalarial drug chloroquine on Plasmodium falciparum.Das B, Gupta R, Madhubala R Pharmacol Res. 1995 Mar-Apr;31(3-4):189-93

70h. Irreversible inhibition of S-adenosylmethionine decarboxylase in Plasmodium falciparum-infected erythrocytes: growth inhibition in vitro.Wright PS, Byers TL, Cross-Doersen DE, McCann PP,Bitonti AJ Biochem Pharmacol. 1991 Jun 1;41(11):1713-8

70i. Antimalarial polyamine analogues.Edwards ML, Stemerick DM, Bitonti AJ, Dumont JA,McCann PP, Bey P, Sjoerdsma A J Med Chem. 1991 Feb;34(2):569-74

70j. Plasmodium falciparum and Plasmodium berghei:effects of ornithine decarboxylase inhibitors on erythrocytic schizogony.Bitonti AJ, McCann PP, Sjoerdsma A Exp Parasitol. 1987 Oct;64(2):237-43

70k. Ornithine decarboxylase of Plasmodium falciparum:a peak-function enzyme and its inhibition by chloroquine.Knigt E, Putfarken B Trop Med Parasitol. 1985 Jun;36(2):81-4

70L. Ornithine decarboxylase inhibition and the malaria-infected red cell:a model for polyamine metabolism and growth.Whaun JM, Brown ND J Pharmacol Exp Ther. 1985 May;233(2):507-11

71a. Polyamine oxidase in human retroplacental serum inhibits the growth of Plasmodium falciparum.Egan JE, Haynes JD, Brown ND, Eisemann CS Am J Trop Med Hyg. 1986 Sep;35(5):890-7

71b. The effect of purified aminoaldehydes produced by polyamine oxidation on the development in vitro of Plasmodium falciparum in normal and glucose-6-phosphate-dehydrogenase-deficient erythrocytes.Morgan DM, Bachrach U, Assaraf YG, Harari E, Golenser J Biochem J. 1986 May 15;236(1):97-101

71c. Polyamine oxidase-mediated intraerythrocytic killing of Plasmodium falciparum: evidence against the role of reactive oxygen metabolites.Rzepczyk CM, Saul AJ, Ferrante A Infect Immun. 1984 Jan;43(1):238-44

71d. Polyamine oxidase mediates intra-erythrocytic death of Plasmodium falciparum.Ferrante A, Rzepczyk CM, Allison AC Trans R Soc Trop Med Hyg. 1983;77(6):789-91

71e. Reactive oxygen and nitrogen intermediates and products from polyamine degradation are Babesiacidal in vitro.Johnson WC, Cluff CW, Goff WL, Wyatt CR Ann N Y Acad Sci. 1996 Jul 23;791:136-47

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74a. Transfer of purines from liver to erythrocytes.In vivo and in vitro studies.Konishi Y, Ichihara A J Biochem (Tokyo). 1979 Jan;85(1):295-301

75a. Nucleoside transport as a potential target for chemotherapy in malaria.Baldwin SA, McConkey GA, Cass CE, Young JD Curr Pharm Des. 2007;13(6):569-80

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75c. Hypoxanthine depletion induced by xanthine oxidase inhibits malaria parasite growth in vitro.Berman PA, Human L Adv Exp Med Biol. 1991;309A:165-8

76a. Molecules targeting the purine salvage pathway in Apicomplexan parasites.Ghacrardi A, Sarciron ME Trends Parasitol. 2007 Aug;23(8):384-9

76b. Nucleoside transport as a potential target for chemotherapy in malaria.Baldwin SA, McConkey GA, Cass CE, Young JD Curr Pharm Des. 2007;13(6):569-80

76c. The plasma membrane permease PfNT1 is essential for purine salvage in the human malaria parasite Plasmodium falciparum.El Bissati K, Zufferey R, Witola WH, Carter NS, Ullman B,Ben Mamoun C Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9286-91

76d. Purine metabolism by the avian malarial parasite Plasmodium lophurae.Yamada KA, Sherman IW Mol Biochem Parasitol. 1981 Aug;3(4):253-64

76e. Purine metabolism during continuous erythrocyte culture of human malaria parasites (P. falciparum).Webster HK, Whaun JM Prog Clin Biol Res. 1981;55:557-73

76f. Purine base and nucleoside uptake in Plasmodium berghei and host erythrocytes.Hansen BD, Sleeman HK, Pappas PW J Parasitol. 1980 Apr;66(2):205-12

76g. Comparison of tritiated hypoxanthine, adenine and adenosine for purine-salvage incorporation into nucleic acids of the malarial parasite, Plasmodium berghei.Van Dyke K Tropenmed Parasitol. 1975 Jun;26(2):232-8

76h. Purine uptake and utilization by the avian malaria parasite Plasmodium lophurae. Tracy SM, Sherman IWJ Protozool. 1972 Aug;19(3):541-9

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77a. Targeting purine and pyrimidine metabolism in human apicomplexan parasites.Hyde JE Curr Drug Targets. 2007 Jan;8(1):31-47

77b. Purine-less death in Plasmodium falciparum induced by immucillin-H, a transition state analogue of purine nucleoside phosphorylase.Kicska GA, Tyler PC, Evans GB, Furneaux RH, Schramm VL,Kim K J Biol Chem. 2002 Feb 1;277(5):3226-31

77c. Structure-activity relationships and inhibitory effects of various purine derivatives on the in vitro growth of Plasmodium falciparum.Harmse L, van Zyl R, Gray N, Schultz P, Leclerc S,Meijer L, Doerig C, Havlik I Biochem Pharmacol. 2001 Aug 1;62(3):341-8

77d. In vitro susceptibilities of Plasmodium falciparum to compounds which inhibit nucleotide metabolism.Queen SA, Jagt DL, Reyes P Antimicrob Agents Chemother. 1990 Jul;34(7):1393-8

77e. Synthesis of adenosine nucleotides from hypoxanthine by human malaria parasites (Plasmodium falciparum)in continuous erythrocyte culture:inhibition by hadacidin but not alanosine.Webster HK, Whaun JM, Walker MD, Bean TL Biochem Pharmacol. 1984 May 1;33(9):1555-7

77f. Hypoxanthine metabolism by human malaria infected erythrocytes: focus for the design of new antimalarial drugs.Webster HK, Wiesmann WP, Walker MD, Bean T, Whaun JM Adv Exp Med Biol. 1984;165 Pt A:219-23

77g. Antimalarial properties of bredinin.Prediction based on identification of differences in human host-parasite purine metabolism.Webster HK, Whaun JM J Clin Invest. 1982 Aug;70(2):461-9

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79a. Controlled clinical evaluations of chlorine dioxide,chlorite and chlorate in man.Lubbers JR, Chauan S, Bianchine JR Environ Health Perspect. 1982 Dec;46:57-62

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79f. Effect of chlorine dioxide water disinfection on hematologic and serum parameters of renal dialysis patients.Ames RG, Stratton JW Arch Environ Health. 1987 Sep-Oct;42(5):280-5

79g. The effects of chronic administration of chlorine dioxide,chlorite and chlorate to normal healthy adult male volunteers.Lubbers JR, Chauhan S, Miller JK, Bianchine JR J Environ Pathol Toxicol Oncol. 1984 Jul;5(4-5):229-38

79h. Effects of the acute rising dose administration of chlorine dioxide, chlorate and chlorite to normal healthy adult male volunteers.Lubbers JR, Bianchine JR.J Environ Pathol Toxicol Oncol. 1984 Jul;5(4-5):215-28

79i. Controlled clinical evaluations of chlorine dioxide,chlorite and chlorate in man.Lubbers JR, Chauhan S, Bianchine JR Fundam Appl Toxicol. 1981 Jul-Aug;1(4):334-8

80a. The effects of chlorine dioxide and sodium chlorite on erythrocytes of A/J and C57L/J mice.Moore GS, Calabrese EJ J Environ Pathol Toxicol. 1980 Sep;4(2-3):513-24

80b. Subchronic toxicity of chlorine dioxide and related compounds in drinking water in the nonhuman primate.Bercz JP, Jones L, Garner L, Murray D, Ludwig DA, Boston J Environ Health Perspect. 1982 Dec;46:47-55

80c. Oxidative damage to the erythrocyte induced by sodium chlorite, in vivo.Heffernan WP, Guion C, Bull RJ J Environ Pathol Toxicol. 1979 Jul-Aug;2(6):1487-99

80d. Acute and chronic toxicity of chlorine dioxide (ClO2)and chlorite (ClO2-) to rainbow trout (Oncorhynchus mykiss).Svecevicius G, Syvokiene J, StasiÅnaite P, Mickeniene L Environ Sci Pollut Res Int. 2005 Sep;12(5):302-5

80e. The kinetics of chlorite and chlorate in rats.Abdel-Rahman MS, Couri D, Bull RJ J Environ Pathol Toxicol Oncol. 1985 Sep-Oct;6(1):97-103

80f. Teratologic evaluation of Alcide liquid in rats and mice. I.Skowronski GA, Abdel-Rahman MS, Gerges SE, Klein KM J Appl Toxicol. 1985 Apr;5(2):97-103

80g. Effects of Alcide gel on fetal development in rats and mice. II.Gerges SE, Abdel-Rahman MS, Skowronski GA, Von Hagen S J Appl Toxicol. 1985 Apr;5(2):104-9

80h. Biochemical interactions of chlorine dioxide and its metabolites in rats.Suh DH, Abdel-Rahman MS, Bull RJ Arch Environ Contam Toxicol. 1984 Mar;13(2):163-9

80i. Pharmacokinetics of Alcide, a germicidal compound in rat.Scatina J, Abdel-Rahman MS, Gerges SE, Alliger H J Appl Toxicol. 1983 Jun;3(3):150-3

80j. Effect of chlorine dioxide and its metabolites in drinking water on fetal development in rats.Suh DH, Abdel-Rahman MS, Bull RJ J Appl Toxicol. 1983 Apr;3(2):75-9

80k. Metabolism and pharmacokinetics of alternate drinking water disinfectants.Abdel-Rahman MS, Couri D, Bull RJ Environ Health Perspect. 1982 Dec;46:19-23

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80m. Toxicological effects of chlorite in the mouse. Moore GS, Calabrese EJ Environ Health Perspect. 1982 Dec;46:31-7

80n. Chlorine dioxide metabolism in rat.Abdel-Rahman MS, Couri D, Jones JD J Environ Pathol Toxicol. 1979 Dec;3(1-2):421-30

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81a. Acute sodium chlorite poisoning associated with renal failure.Lin JL, Lim PS Ren Fail. 1993;15(5):645-8

82a. First-aid reports of acute chlorine gassing among pulpmill workers as predictors of lung health consequences.Salisbury DA, Enarson DA, Chan-Yeung M, Kennedy SM Dep. Med., Respiratory Div., Univ. B.C., 2775 Heather St.,Vancouver, B.C. V5Z 3J5, Canada Am J Ind Med; (1991) 20(1):71-82

82b. Health Effects of Working in Pulp and Paper Mills:Exposure, Obstructive Airways Diseases,Hypersensitivity Reactions, and Cardiovascular Diseases.Toren K, Hagberg S, Westberg H American Journal of Industrial Medicine, 29(2):111-122, 75 references, 1996.

82c. Reactive Airways Dysfunction Syndrome Due to Chlorine [Dioxide]: Sequential Bronchial Biopsies and Functional Assessment Lemiere C, Malo J-L, Boutet M European Respiratory Journal, 1997, 10(1):241-244,

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82e. Chlorine Dioxide. HSE. Risk assessment document.Volume EH72/14 (2000) 61 pages. Occupational exposure.

82f. Respiratory effects of industrial chlorine and chlorine dioxide exposure. [academic dissertation]Grenquist-Nordâen B Institute of Occupational Health,University of Helsinki, Haartmaninkatu 1, Helsinki, Finland,1983, 83pages

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83a. The effects of chronic administration of chlorite to glucose-6-phosphate dehydrogenase deficient healthy adult male volunteers.Lubbers JR, Chauhan S, Miller JK, Bianchine JR J Environ Pathol Toxicol Oncol. 1984 Jul;5(4-5):239-42

83b. G6PD-deficiency: a potential high-risk group to copper and chlorite ingestion. Moore GS, Calabrese EJ J Environ Pathol Toxicol. 1980 Sep;4(2-3):271-9

83c. Groups at potentially high risk from chlorine dioxide treated water.Moore GS, Calabrese EJ, Ho SC J Environ Pathol Toxicol. 1980 Sep;4(2-3):465-70

83d. G6PD-deficiency: a potential high-risk group to copper and chlorite ingestion.Moore GS, Calabrese EJ J Environ Pathol Toxicol. 1980 Sep;4(2-3):271-9

83e. Potential health effects of chlorine dioxide as a disinfectant in potable water supplies.Moore GS, Calabrese EJ, DiNardi SR, Tuthill RW Med Hypotheses. 1978 Sep-Oct;4(5):481-96

83f. [G6PD phenotype and red blood cell sensitivity to the oxidising action of chlorites in drinking water]Contu A, Bajorek M, Carlini M, Meloni P, Cocco P, Schintu M Ann Ig. 2005 Nov-Dec;17(6):509-18 [Article in Italian]

83g. Effects of environmental oxidant stressors on individuals with a G-6-PD deficiency with particular reference to an animal model.Calabrese EJ, Moore G, Brown R Environ Health Perspect. 1979 Apr;29:49-55

84a. The effects of chronic administration of chlorite to glucose-6-phosphate dehydrogenase deficient healthy adult male volunteers.Lubbers JR, Chauhan S, Miller JK, Bianchine JR J Environ Pathol Toxicol Oncol. 1984 Jul;5(4-5):239-42

84b. [G6PD phenotype and red blood cell sensitivity to the oxidising action of chlorites in drinking water]Contu A, Bajorek M, Carlini M, Meloni P, Cocco P, Schintu M Ann Ig. 2005 Nov-Dec;17(6):509-18 [Article in Italian]

85a. Estimation of the total parasite biomass in acute falciparum malaria from plasma PfHRP2. Dondorp AM, Desakorn V, Pongtavornpinyo W, Sahassananda D,Silamut K, Chotivanich K, Newton PN, Pitisuttithum P,Smithyman AM, White NJ, Day NP PLoS Med. 2005 Aug;2(8):e204;Epub 2005 Aug 23 Erratum in: PLoS Med. 2005 Oct;2(10):390 Comment in: PLoS Med. 2006 Jan;3(1):e68; Author reply e69.

86a. Current status and progresses made in malaria chemotherapy.Liatares GE, Rodriguez JB Curr Med Chem. 2007;14(3):289-314

87a. Toxoplasma gondii: the model apicomplexan.Kim K, Weiss LM Int J Parasitol. 2004 Mar 9;34(3):423-32

88a. Sequential inactivation of Cryptosporidium parvum oocysts with chlorine dioxide followed by free chlorine or monochloramine.Corona-Vasquez B, Rennecker JL, Driedger AM, Mariñas BJ Water Res. 2002 Jan;36(1):178-88

89a. Characterization of an omega-class glutathione-S-transferase from Schistosoma mansoni with glutaredoxin-like dehydroascorbate reductase and thiol transferase activities.Girardini J, Amirante A, Zemzoumi K, Serra E Eur J Biochem. 2002 Nov;269(22):5512-21

89b. Thiol-based redox metabolism of protozoan parasites.Muller S, Liebau E, Walter RD, Krauth-Siegel RL Trends Parasitol. 2003 Jul;19(7):320-8 Comment in: Trends Parasitol. 2004 Feb;20(2):58-9

89c. The parasite-specific trypanothione metabolism of trypanosoma and leishmania.Krauth-Siegel RL, Meiering SK, Schmidt H Biol Chem. 2003 Apr;384(4):539-49

89d. The synthesis of parasitic cysteine protease and trypanothione reductase inhibitors.Chibale K, Musonda CC Curr Med Chem. 2003 Sep;10(18):1863-89

89e. Glutathione inhibits the antischistosomal activity of artemether.Zhai ZL, Jiao PY, Mei JY, Xiao SH Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi.2002;20(4):212-5

89f. Schistosoma mansoni: expression and role of cysteine proteinases in developing schistosomula.Zerda KS, Dresden MH, Chappell CL  Exp Parasitol. 1988 Dec;67(2):238-46

89g. Mr 26,000 antigen of Schistosoma japonicum recognized by resistant WEHI 129/J mice is a parasite glutathione S-transferase.Smith DB, Davern KM, Board PG, Tiu WU, Garcia EG, Mitchell GF Proc Natl Acad Sci U S A. 1986 Nov;83(22):8703-7 Erratum in: Proc Natl Acad Sci U S A 1987 Sep;84(18):6541

89h. Oxidative stress and antioxidant defenses:a target for the treatment of diseases caused by parasitic protozoa.Turrens JF Mol Aspects Med. 2004 Feb-Apr;25(1-2):211-20

89i. Antioxidant defense mechanisms in parasitic protozoa.Mehlotra RK Crit Rev Microbiol. 1996;22(4):295-314

89j. Phenotypic analysis of trypanothione synthetase knockdown in the African trypanosome.Ariyanayagam MR, Oza SL, Guther ML, Fairlamb AH Biochem J. 2005 Oct 15;391(Pt 2):425-32

89k. Gene knockdown of gamma-glutamylcysteine synthetase by RNAi in the parasitic protozoa Trypanosoma brucei demonstrates that it is an essential enzyme.Huynh TT, Huynh VT, Harmon MA, Phillips MA J Biol Chem. 2003 Oct 10;278(41):39794-800

89L. Polyamine and thiol metabolism in Trypanosoma granulosum: similarities with Trypanosoma cruzi.Mastri C, Thorborn DE, Davies AJ, Ariyanayagam MR,Hunter KJ Biochem Biophys Res Commun. 2001 Apr 20;282(5):1177-82

89m. Inducible resistance to oxidant stress in the protozoan Leishmania chagasi.Miller MA, McGowan SE, Gantt KR, Champion M,Novick SL, Andersen KA, Bacchi CJ, Yarlett N,Britigan BE, Wilson ME J Biol Chem. 2000 Oct 27;275(43):33883-9

89n. Pharmacological approaches to antitrypanosomal chemotherapy.Croft SL Mem Inst Oswaldo Cruz. 1999 Mar-Apr;94(2):215-20

89o. Fate of soluble methionine in African trypanosomes:effects of metabolic inhibitors.Bacchi CJ, Goldberg B, Garofalo-Hannan J, Rattendi D,Lyte P, Yarlett N Biochem J. 1995 Aug 1;309 ( Pt 3):737-43

89p. In vivo effects of difluoromethylornithine on trypanothione and polyamine levels in bloodstream forms of Trypanosoma brucei.Fairlamb AH, Henderson GB, Bacchi CJ, Cerami A

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