WIKI-MEDICAL
A Medical Encyclopedia Dedicated to the Matters of Science, Health, and Healing

 
Welcome
Vision and Mission
Why Should You Use Wiki-Medical?
Founder
Molecular Biology of Oxygen, Basic
Molecular Biology of Oxygen, Advanced
Insulin-Obesity-Diabetes
Nutrition
Environment
Energy Healing
Cardiovascular (CVS)
Pulmonary
Gastrointestinal (GI)
Endocrine
Urinary
Reproductive System
Brain
Musculo-sketal
Philosophy
History
Medical Ethics
Children's Learning Fields
Lap Dog Journalists

 

HYDROGEN PEROXIDE THERAPIES:

RECENT INSIGHTS INTO OXYSTATIC AND ANTIMICROBIAL ACTIONS

Majid Ali, M.D.

My colleagues at the Institute and I routinely prescribe hydrogen peroxide foot soaks for patients with acute and chronic lower leg edema caused by peripheral arterial insufficiency, varicose veins, unresolved trauma, low-grade chronic infectious and atopic processes. Based on clinical results obtained in several hundred patients, I now consider this therapy (described later in this article) to be the safest and most effective therapy for those conditions.

We have also prescribed intravenous hydrogen peroxide infusions for over 3,000 patients with varying degrees of respiratory-to-fermentative (RTF) shift in ATP generation associated with chronic fatigue states.1,2 Based on that experience, we now consider that therapy as one of the safest and most effective therapies for such patients. The long-term clinical outcomes of integrative protocols with focus on hydrogen peroxide infusions have been published.3 In this article, I briefly review some basic aspects of hydrogen peroxide chemistry and therapeutics, and then present newer information about hydrogen peroxide signaling that sheds light on the molecular mechanisms that explain our clinical observations.

Discovery and Natural Occurrence

Hydrogen peroxide was discovered in 1818 by the French chemist Louis-Jacques Thenard. He coined the term eau oxygenee, to express his belief that it was an oxygenated form of oxygen. It is not clear if he fully understood the enormous medical significance of his discovery. Hydrogen peroxide is colorless, heavier than water, and has a larger liquid range than water, the melting point ranging from -11C (70%) to -39C (70%). It is produced within the plant biomass and plays diverse and pivotal roles in the cellular communication and energetic systems in the plant kingdom. It is present in trace amounts both in rainwater and snow. Interestingly, it is found in higher concentrations in natural spring waters of many healing shrines, most notably in Lourdes in France, Fatima in Portugal, and St. Anne's in Quebec. In light of my observations of the clinical benefits of H2O2 therapies in a host of clinical entities, I am tempted to speculate that many of the putative benefits of the shrine waters accrue from the oxystatic roles of H2O2. It is also likely that the mineral compositions of such waters enhance their oxystatic benefits.

Hydrogen Peroxide: A Misunderstood Molecule

Hydrogen peroxide is a misunderstood molecule. It is a potent in vitro oxidant. And yet, it serves as an effective in vivo antioxidant in clinical states associated with chronic accelerated oxidative molecular stress.4,5 It is procoagulant under certain conditions and anticoagulant under others.6 It is proinflammatory in some roles and anti-inflammatory in others.7 It induces some genes and suppresses others.8,9 It is a critically important second messenger in many pathways. 10-14 It is procancer in some aspects and anti-cancer in others.

Hydrogen peroxide plays multiple Dr. Jekyll/Mr. Hyde roles in enzymatic dynamics of the body, inducing some and impairing the functions of others,15-19 including: (1) inactivation of xanthine oxidase by reactions that involve formation of hydroxyl radicals; (2) oxidation of the oxidation-sensitive thiol groups at the active site of glucose-3-phosphate dehydrogenase and so inhibits the enzyme, thus reducing ATP-dependent synthesis of many proteins; (3) inhibition of glyceraldehyde phosphate dehydrogenase (GAPDH), providing a mechanism by which hydrogen peroxide exerts a regulatory effect on endothelial pathophysiology; (4) regulation of activities of crucial energy enzymes, such as sodium-potassium ATPase18; activation of potent enzymatic antioxidant defenses, including glutathione peroxidase.19 Other important metabolic aspects of hydrogen peroxide include: (1) hexose monophosphate shunt20; (2) mitochondrial enzymatic pathways21; (3) enzymes of membrane transport systems22; (4) thyroglobulin iodinases23; (5) prostaglandin synthesis24; (6) bioamine metabolic pathways, including those of norepinephrine, dopamine, and serotonin25; and (7) progesterone and estrogenic synthetic pathways.26 By those and other roles, hydrogen peroxide activates a host of oxyenzymes—enzymes that are directly involved in oxygen homeostasis—and alters the expression of oxygenes in many ways.

The Beginning of H2O2 Therapeutics

In 1898, Cortelyou of Marietta, Georgia, reported successful results obtained in patients with disorders of the nose and throat.27 In the same year, I.N. Love reported his successful use of H2O2 for treating scarlet fever, diphtheria, pneumonia, and uterine cancer in the Journal of the American Medical Association.28 A clear record of what appears to be the first clinical use of intravenously administered hydrogen peroxide appeared in an article published in Lancet in 1920 by Oliver and Cantab.29 They were military physicians treating Indian Gurkha soldiers. During an influenza epidemic, they encountered 80% mortality among soldiers who developed pneumonia. In desperation—possibly emboldened by a lack of fear of serious censure if the treatment were to be fatal for some terminally ill Indian soldiers—they undertook intravenous infusions of hydrogen peroxide to treat pneumonia. They were fortunate. In their landmark paper, they reported more than 50% reduction in mortality — 13 of 25 treated soldiers survived! There were no cases with clinical or pathologic evidence of air embolism. It puzzles me why that report was not followed by widespread use of that treatment of pneumonia in Britain.

A pioneer of intravenous H2O2 therapy was Charles Farr. During the mid-1990s, he honored me by having me serve as his co-director of courses on bio-oxidative therapies. Farr made several important original clinical and experimental observations about intravenous hydrogen peroxide infusions. He documented short-term and long-term effects of that therapy on various aspects of the immune system. One of his astute observations concerned the dramatic changes—up to 100% increase from the pre-infusion levels—in oxygen consumption rate. He clearly established the fact that biologic effects of that therapy cannot be merely attributed to the miniscule amounts of oxygen liberated from the infused hydrogen peroxide.30

Mechanisms by Which H2O2 Improves Arterial, Venous, and Lymphatic Circulations

A large number of short-term and long-term observations have convinced us that H2O2 improves arterial, venous, and lymphatic circulation. Those effects are mediated by a host of mechanisms. Personal morphologic observations with phase-contrast microscopy have convinced me that the most important of those mechanisms is control of oxidative coagulopathy by myriad molecular mechanisms listed below. Microclots and microplaques in the circulating blood are readily detected by examination of freshly prepared and unstained smears of the peripheral circulating blood with high-resolution, phase-contrast microscopy.31-33 The arrest of oxidative lymphopathy occurs concurrently with control of oxidative coagulopathy, though a suitable lymph specimen for direct documentation of that phenomenon is generally not forthcoming.

The primary mechanism by which H2O2 exerts those circulatory effects is proteolytic dissolution of microclots and microplaques in the vascular channels. Less important effects of H2O2 include the following: (1) peripheral vasodilatation34; (2) coronary vasodilatation35; (3) cerebral arteriolar dilatation36; and (4) pulmonary vasodilatation37; and (5) peripheral vasodilatation.36

H2O2 and Phagocytosis

Antimicrobial properties of hydrogen peroxide were recognized soon after its discovery. It was to be expected that the seminal work of the Russian biologist, Elie Metchnikoff, concerning humoral immunity during the late nineteenth century would also bring hydrogen peroxide into sharper focus. That, indeed, happened. The classical concept of phagocytic microbial killing may be summarized as follows38-43: (1) The invading microbes are exposed to serum factors, opsonized, and engulfed within the phagocytic cells; (2) The engulfed microbes are encapsulated by a series of fusion processes culminating in the development of the mature phagosome41; (3) Phagosomes merge with early endosomes to increase the vesicle size; (4)Membrane-bound vacuolar ATPases and proteolytic enzymes necessary for particle and microbial degradation are acquired42; (5) Bactericidal molecular machinery of cytoplasmic granules is brought into action with the release of their granules; and (6) Actual demise of microbes is attributed to production of free radicals—superoxide, hydrogen peroxide, and others—during respiratory burst.

H2O2, Matrix Regulation, and Microbial Killing

Recent studies have revealed that actual molecular dynamics of microbial killing are far more complex than simple destruction of mirobes by free radicals.44,45, 46 Specifically, certain conditions of the granular matrix are essential for completing the process of microbial disintegration. The matrix within the granules is highly charged. Granular proteases are normally adsorbed to it in an inactive form. When the ionic strength in the vacuoles rises, the enzymes are activated and unleashed to serve their microbiocidal roles. Those enzymes function optimally at elevated pH levels which exist in the vacuoles under those conditions. The respiratory burst within the phagocytic vacuoles is accompanied by a surge in the intravacuolar pH—from 6 to nearly 8. A large influx of potassium ions through the vacuolar membrane occurs and offsets the anionic charge. That happens in spite of the release of predominantly acidic granular contents since protons are consumed in neutralizing the excess of basic superoxide ions and other radicals.47

Concurrently, osmotically potent degradation products are released from disintegrating microbes, rendering the vacuole markedly hypertonic and shrinking the viable bacteria by as much as 50%. Such microbial shrinking is prevented if protease inhibitors are introduced into the system. Undue expansion of the vacuoles is prevented by a dense network of membrane cytoskeletal proteins.

Neutrophilic myeloperoxidase, itself capable of destroying microbes, appears to protect proteases from oxidative damage, to which they are vulnerable, especially cathepsin G.48

The Role of Potassium Ions

The passage of electrons across the vacuolar membrane is electrogenic. Specifically, the superoxide-generating NADPH oxidase of human neutrophils is electrogenic and is associated with an H+ channel.49 There are important changes in H+ dynamics during phagocytosis. For example, protein C kinase activates an H+-(equivalent) conductance in the plasma membrane of human neutrophils. Activation of NADPH oxidase-related proton and electron currents occurs simultaneously in human neutrophils. Potassium ions play a central role in the microbial killing process. Oxidases generate a potential difference across the membrane. Potassium ions move to compensate for that difference and in doing so enable the pH to rise to a level necessary for optimal function of proteases. Potassium ions activate granule enzymes. When phagocytes are inactive (not engulfing and killing microbes), the granules contain a strongly anionic sulfated proteoglycan matrix that binds tightly to cationic proteases. In the bound form, proteases cannot digest microbes. There is evidence that hypertonic K+ driven into vacuoles by NADPH oxidase is responsible for unleashing (by solubilizing) those enzymes, since elevated pH on its own is unable to activate proteases. 50

Would one expect the other ionic channels to sit out the action of phagocytosis? Hardly, in view of Nature's preoccupation with complementarity and contrariety. Free calcium ions initiate, augment, or perpetuate an enormous variety of cellular processes. For example, calcium is involved with coupling of diverse stimuli to their respective specific responses,51,52 including: (1) light; (2) touch; (3) gravity; (4) cold shock; (5) hormones; (6) bacterial compounds; and (7) mycotoxins. Stimulus specificity appears to be encoded through a multitude of Ca2+ mobilization pathways. For example, vacuolar ligand-gated Ca2+ mobilization pathways may involve both Ca2+- and voltage-operated Ca2+ release channels in the same membrane, acting singly or coordinately. Directly or indirectly, such calcium-related responses are involved in nearly all crucial steps in phagocytosis. Not unexpectedly, many of the specific calcium responses depend on their spatio-temporal concentrations. To render the calcium-related cellular happenings yet more fascinating, some nuclear processes appear to be executed in response to an autonomously regulated nuclear calcium signal. It may be added parenthetically that chloride ions also play a role in phagocytic dynamics. Specifically, chloride efflux regulates adherence, spreading, and respiratory burst of neutrophils stimulated by tumor necrosis factor-á (TNF) on biologic surfaces.53

In discussion of the structure and function of the matrix, little, if any, attention is given to the matrix within the cell as well as within cellular organelles. And yet, the matrix in those locations serves key redox metabolic and defense roles. The complexities in the phagocytic destruction of microbes should not be surprising because Nature, first and foremost, has to protect cells and vacuoles from the self-destructive impulses of their own enzymatic arsenals. An enormous number of phagocytic cells infiltrate the inflamed tissues invaded by microbes. Such cells deliver a huge load of autolytic enzymes fully capable of damaging autologous tissues. Thus, the 'packaging' of the enzymes provides the needed defense against self-inflicted injury triggered by free radical sparks. It may be added here that the matrix of phagocytic granules — seldom a point of focus — also plays a central role in destruction of microbes after phagocytosis.

 

Table 1. Composition of Hydrogen Peroxide - I

Nutrient

Concentration

Volume

Hydrogen peroxide

3.75%

0.35 ml

Sodium Bicarbonate

0.5 mEq/ml = 1.25 mEq

2.5 ml

Normal saline 0.9%

 

150 ml

 

 

Table 2. HYDROGEN PEROXIDE-II

(Hydrogen Peroxide-I Followed By Infusion Given Below In 30-45 Minutes

Nutrient

Concentration

Volume

Magnesium sulfute.

500 mg/ml =1.5 ml

750 mg

Zinc

5 mg/ml = 2 ml

12 mg

Calcium gly/lac

10 mg/ml = 7.5 ml

75 mg

Pantothenic acid

250 mg/ml = 1.5 ml

375 mg

Pyridoxine

100 mg/ml = 1 ml

100 mg

Vitamin C

500 mg/ml = 1 ml

0.5 gm

Vit. B Complex

*

1 ml

Molybdenum

25 mcg/ml = 5 ml

125 mcg

Sodium Bicarbonate

2.5 mEq/5 ml = 1.5 ml

---------

Lidocaine

20 mg/ml = 1.5 ml

30 mg

0/45% Saline

 

50 ml

 

I might point out here that matrix proteases perform the microbial killing rituals, but oxygen and the oxygen-driven oxidative phenomena provide the initial sparks.

Protocol for Hydrogen Peroxide Foot

Soaks and Baths

Hydrogen peroxide soaks can be used with different concentrations of and H2O2 and salt. The following is the standard protocol prescribed at the Institute protocol:

H2O2 Soaks Protocol

.  Water 20 parts

.  H2O2 3% 1 part

.  Salt One teaspoon

.  Time 20 minutes

The recommended choices of salt are as follow: (1) Epsom salt; (2) sea salt; and (3) common table salt.

Stronger solutions of H2O2, such as one part of H2O2 and 10 parts of water or 1 part of H2O2 and 15 parts of water may also be tried to test for variations in efficacy for individual persons.

For chronic conditions, I generally prescribe foot soaks on a four or five day a week basis. For subacute conditions, daily soaks are recommended. Uncommonly, I have prescribed such soaks on a twice daily basis.

There are several good brands of foot soak and foot massage units available on the market. The one made by Brookstone Company creates effective whirlpool conditions and includes a "nodule" for effective massaging of tender points on the feet or ankles.

Related Tutorials

* Molecular Biology of Oxygen Advanced

* HYDROGEN PEROXIDE THERAPIES:

 

References

1. Ali M. Oxygen and Aging. (Ist ed.) New York, Canary 21 Press. Aging Healthfully Book 2000.

2. Efficacy of ecologic-integrative management protocols for reversal of fibromyalgia: an open prospective study of 150 patients. J Integrative Med 1999; 3:48-64.

3. Ali M. Ali M. The Principles and Practice of IntegrativeMedicine Volume III: Dysoxygenosis and Oxystatic Therapies. 2003. Washington, D.C. Capital University Press (in collaboration with Canary 21 Press, New York). www.cuim.edu & www.Canary21press.com)

4. Farr CH. The Therapeutic Use of Intravenous Hydrogen Peroxide (Monograph). 1987. Oklahoma City, Genesis Medical Center.

5. Altman N. Oxygen Healing Therapies for Optimal Health & Vitality. 1995. Rochester, Vermont. Healing Arts Press.

6. Polgar P, Taylor L. Stimulation of prostaglandin synthesis by ascorbic acid via lydrogen peroxide formation. Prostag 1980;19:693.

7. Agrawal P, Harper MJ: Studies on peroxidase catalyzed formation of progesterone. Steroids 1982;40:569-572.

8. McFaul SJ. The mechanism of peroxidase-mediated cytotoxicity. Comparison of horseradish peroxidase and lactoperoxidase. Proc Soc Exp Biol Med 1986;182:244-249.

9. Yamaja Setty BN, Jurek E. Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.

10. Ward JF, Blakey WF, Joner EL. Mammalian cells are not killed by DNA single-strand breaks caused by hydroxyl radicals from hydrogen peroxide endothelial cells against oxidant damage. Biochem Biophys Res Commun 1985;127-270-276.

11. Xu Y, Mayne L, Englander SW. Evidence for an unfolding and refolding pathway in cytochrome c. Nature Structural Biology. 1998;5:774-778.

12. Chen Y-R, Shrivastava A, Tan T-H. Down-regulation of the c-Jun N-terminal kinase (JNK) phosphatase M3/6 and activation of JNK by hydrogen peroxide and pyrrolidine dithiocarbamate. Oncogene. 2001;20,367-374.

13. Steiner BM, Wong GH, Sutrave P, et al. Oxygen toxicity in Treponema pallidum: Deoxyribonucleic acid single- stranded breakage induced by low doses of hydrogen peroxide. Can J Microbiol. 1984;30:1467-76.

14. Boyington JC, Motyka SA, Schuck P, et al. Crystal structure of an NK cell immunoglobulin-like receptor in complex with its class I MHC ligand. Nature. 2000;405:537-543.

15. Gorren AC, Dekker H, Weaver R. Kinetic investigations of the reactions of cytochrome C oxidase with hydrogen peroxide. Biochem Biophys Acta 1986;852:81-92.

16. D 46 Yamaja Setty BN, Jurek E, Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.

17. Polgar P, Taylor L. Stimulation of prostaglandin synthesis by ascorbic acid via hydrogen peroxide formation. Prostag 1980;19:693.

18. Del Maestro RF, Thaw HH, Bjork J, et al. Free radicals as mediators of tissue injury. Acta Physiol Scand 1980;492:43-57.

19. Babior BM, Kipnes RS, Curnutte JT. Biological defense mechanisms: the production by leukocytes of superoxide, a potential bactericidal agent. J Clin Invest 1973;52:741-744.

20. Hothersall JD, Greenbaum AL, McLean P. The functional significance of the pentose phosphate pathway in synaptosomes: Protection against peroxidative damage by catecholamines and oxidants. J Neurochem 1982;39:13252.

21. Eto K, Tsubamoto Y, Terauchi Y, et al. Role of NADH shuttle system in glucose-induced activation of mitochondrial metabolism and insulin secretion. Science. 1999;283:981-5. Also: DesMarias DJ. Science. 2000;289:1703.

22. Verhoeven AJ, Mommersteeg ME, Akkerman JW. Balanced contribution of glycolyte and adenylate pool in supply of metabolic energy.

23. Wildberger E, Kohler H, Jenzer H, et al. Inactivation of peroxidase and glucose oxidase by H202 and iodination. Mol Cell Endocrinol 1986;46:149-154.

24. Zoschke DC, Staite ND. Suppression og human lymphocyte proliferation by activate neutrophils or H202. Surviving cells have an altered T Helper/T Suppressor ratio and an increased resistance to secondary oxidant exposure. Clin Immunol Immunopathol 1987;42:160-170.

25. Heikkila R, Cohen G. Inhibition of biogenic amine uptake by hydrogen peroxide: A Mechanism for toxic effects of 6-hydroxydopamine. Science 1971;172:1257-1258.

26. Agrawal P, Harper MJ: Studies on peroxidase catalyzed formation of progesterone. Steroids 1982;40:569-572.

27. Douglas WC. Hydrogen Peroxide Medical Miracle. 1990. Atlanta. Second Opinion Publishing, Inc. (quoted in)

28. Love I. www.cancer.org/docroot/ETO/content /ETO_5_3X_hydrogen_peroxide_therapy.

29. Oliver TH, Cantab BC, Murphy DV. Influenza; pneumonia: the intravenous injection of hydrogen peroxide. Lancet 1920;1:432-433.

30. Farr CH. The Therapeutic Use of Intravenous Hydrogen Peroxide (Monograph). 1987. Oklahoma City, Genesis Medical Center.

31. Ali M: Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome (abstract). Am J Clin Pathol , 94:515,1990.

32. Ali M, Ali O: AA oxidopathy: the core pathogenic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:6-112.

33. Ali M, Ali O: AA oxidopathy: the core pathogenic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:6-112.

34. Farr CH: The therapeutic use of intravenous hydrogen peroxide (Monograph). Genesis Medical Center, Oklahoma City, OK 73120, January 1987.

35. Rubanyi GM, Vanhoutte PM. Oxygen-derived free radicals, endothelium and responsiveness of vascular smooth muscle. Am J physiol 1986;250:(5 pt 2):H815-821.

36. Yamaja Setty BN, Jurek E. Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.

37. Yamaja Setty BN, Jurek E, Ganley C., et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag 1980;19"693.

38. Murray HW, Scavuzzo D, Jacobs JL, et al. In vitro and in vivo activation of human mononuclear phagocytes by interferon-gamma. Studies with normal and AIDS monocytes. J Immunol 1987;138:2457-2462.

39. Powell JH, Shor R, Gazit E, et al. The effects of Con A-induced Lymphokines from the T-lymphocyte subpopulation on human monocyte leishmaniacal capacity and H202 production. Immun 1986;59:245-250.

40. Levine A, Tenhaken R, Dixon R, et al. H202 from the oxidative burst orchestrates the plant hypersensitive response. Cell 1994;79:583-593

41. Yahraus T, Chandra S, Legendre L, et al. Evidence for a mechanically induced oxidative burst. Plant Physiol 1995;109,1259-1266.

42. Gutteridge JM, Wilkins S: Copper salt-dependant hydroxyl radical formation. Damage to proteins acting as antioxidants. Biochim biophys acta 1983;759:38-41.

43. Babior BM, Curnutte JT, Kipnes RS. Biologic defense mechanisms. Evidence for the participation of superoxide in bacterial killing by xanthine oxidase. J Lab Clin Med 1973;52:741-744.

44. Henderson LM, Chappel JB, Jones OT. The superoxide-generating NADPH oxidase of human neutrophils is electrogenic and associated with an H+ channel. Biochem. 1987;246:325-329.

  • 45. Sasada M, Kubo A, Nishimura T, et al. Candidacidal activity of monocyte-derived human macrophages: Relationship between candida killing and oxygen radical generation by human macrophages. J Leukocyte Biol 1987;41:289-294.

  • 46. Zoschke DC, Staite ND. Suppression og human lymphocyte proliferation by activate neutrophils or H202. Surviving cells have an altered T Helper/T Suppressor ratio and an increased resistance to secondary oxidant exposure. Clin Immunol Immunopathol 1987;42:160-170.

    47. Di A, Krupa B, Bindokas VP, et al. Quantal release of free radicals during exocytosis of phagosomes. Nature Cell Biol. 2002;4:279-285.

    48. Burdon RH, Alliangana D. Gill V. Endogenously generated active oxygen species and cellular glutathione levels in relation to BHK-21 cell proliferation. Free Radical Res 1994;21:121-133.

    49. Henderson LM, Chappel JB, Jones OT. The superoxide-generating NADPH oxidase of human neutrophils is electrogenic and associated with an H+ channel. Biochem. 1987;246:325-329.

    50. Gutteridge JM, Wilkins S: Copper salt-dependant hydroxyl radical formation. Damage to proteins acting as antioxidants. Biochim biophys acta 1983;759:38-41.

    51. Zgliczynski JM, Selvaraj RJ, Paul BB, et al. Chlorination by the myeloperoxidase-H202-C1 antimicrobial system at acid and neutral pH. Proc Soc Exp Biol Med 1977;154:

    418-422.

    52. TjelleT, Saigal B, Berg MF. Degradation of phagosomal components in late endocytic organelles. J Cell Sci1998;111:141-148.

    53. Zhu H, Bunn HF. How do cells sense oxygen. Science 2001;292:449-451.

     

    Section Home

    Respiratory ATP

    Hydrogen Peroxide

    Cancer Oxygen

     The Oxygen View of Pain:

     Iraq War-associated sickness

    Bone Homeostasis and osteoporosis