James J Whitehead,
Long term Survivor of hiv/oxidative stress/aids Researcher Continuum Magazine,Member of www.altheal.
40 A Josephine Avenue, london United kingdom
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Dear Nicholas Bennett,
Thank you for the references regarding Kaposi sarcoma. I was aware that Kaposi sarcoma occured in other types of transplant recipients but the reason I specificaly mentioned Kidney transplant recipients was because I was under the impression that Kaposi Sarcoma occured far more frequently amongst kidney transplant recipients. ?
Again I am side stepping the issues about hiv/hhv-8 existance and roles in the pathology of aids and kaposi Sarcoma (KS) "cancer".
Instead I have again concentrated on oxidative stress and glutathione defiency.Whether one believes that the oxidative stress/glutathione defiency is induced by co factors, hiv or both there can be no doubt that oxidative stress and glutathione is pivatol in the pathogenesis
of Aids and Kaposi Sarcoma and there for reducing agents such as S- Acetyl-Glutathione (SAG), NAC and other antioxidants could be used as prevention and treatment of aids , Kaposi Sarcoma and exploited for preventing cancer progression as well as used in cancer adjuvant therapy as well as treating aids wasting.
I have had aids defining Kaposi Sarcoma myself for 3 or 4 years and I have quite abit of personal experiences of friends who have it or have died with it.My Kaposi sarcoma unlike my many friends is very weak small and none aggressive. I went off combination therapy for year and did an intensive course of antioxidants particualy glutathione based ones like S Acetyl Glutathione , NAC, undenurtured whey proteins, Alpha Lipoic Acid as well as a wide spectrum of micro nutrients, antioxidants, and amino acid complexes( to treat aids wasting syndrome). My Kaposi sarcoma legion completley disapeared and went away for months , all that was left was a small white scar where I had the biospi performed, the KS and all redness had gone. However I restarted combo and stopped the antioxidants, my CD4 went from 30 to 130 and my viral load went undectable but I had two small new Kaposi sarcoma legions reapear on my left arm in the same spot where I used to have one within 4 weeks of restarting the combo. I also noticed the appearance off papiloma at the same time. I have been told that this is due to whats called immune reconstition, which say like with other conditions like CMV can be recactivated when immune reconstition is taking place. How common is this ?
I have now restarted antioxidants and had to stop combo because of side effects, but I have also noticed that Kaposi Sarcoma, quite agressive forms are occuring amongst friends of mine who have high CD4's and the Kaposi sarcoma despite combo does not go, some require additional localised therapies, some respond just to combo and you see the KS regress on some but not all. Why is my KS so pathetic, so weak , disapearing, reapearing ? with a low cd4 and yet friends with high cd4 both on and off combo have agressive none disapearing KS ?
www.Altheal.org has both so-called asymptomatic and symptomatic volunteers for clinnical trials into antioxidant therapies both as alternatives and as complementaries and members who are actively seeking medical professionals who will co operate with the treatment choices/wishes in the UK and around the world.
More links and notes (scrap book) on Kaposi Sarcoma cam be found at
"The induction of iatrogenic KS by immunosuppressive therapy and its subsequent regression on removal of immunosuppression provided some of the earliest clinical recognition of the reversibility of KS (216).". (1). "Iatrogenic KS shows extreme ethnogeographic associations, occurring in only about 0.4% of transplant patients in the United States and Western Europe (157, 398) but in about 4.0 to 5.3% of renal transplant patients in Saudi Arabia (399, 411).". (1).
"The incidence of KS in renal transplant recipients varies widely from country to country; figures from 0.4–5.3% have been reported [12,13]".(3).
"Strikingly, KS represents 87.5% of posttransplantation neoplasia in Saudi Arabia (412), and a recent study found KS in 80% of posttransplantation cancers in Turkey (141). In the latter study, KS developed within 1 year in 46% of those cases. The high frequency of iatrogenic KS in Saudi Arabia reflects the 7% endemic seroprevalence of KSHV in healthy Saudi donors or patients with non-KS malignancies (412). Interestingly, transplant-associated KS is seen predominantly in kidney allograft recipients and not other solid-organ or bone marrow transplant recipients (230); kidney recipients have a greater than two-fold-higher seroprevalence than those at low risk of KS in France (85)." .(1).
"Although Andreoni et al. found that 21.4% of liver recipients, but only 8.6% of kidney recipients, seroconverted for KSHV, the risk of KS was higher in the kidney transplant recipients." .(1).
" The incidence of HHV-8/KSHV infection tended to be higher among liver transplant recipients. Four renal transplant recipients and none of the liver transplant recipients developed KS after transplantation.".(2).
"Conclusions: HHV-8/KSHV seroconversion rates appear to be higher among liver transplant recipients, compared to renal transplant recipients. However, renal transplant recipients tend to have a higher risk of KS.".(2).
"Differences in immunosuppressive therapy might favor KSHV reactivation in the kidney recipients" .(1). "HHV-8/KSHV reactivation appears to play a greater role on the risk of KS than incident infections". (2).
"The seroprevalence of KSHV was 79% (63/80) in those with Kaposi's sarcoma as compared to 50% (302/607) in those without (chi(2) heterogeneity (1 df) = 21.0; p < 0.001) and the risk of the tumour increased with increasing anti-KSHV antibody titres (chi(2) trend (1 df) = 29.7; p < 0.001)." .(10).(Risk factors for Kaposi's sarcoma: a case- control study of HIV-seronegative people in Uganda.)
"The risk of Kaposi's sarcoma is clearly linked to antibody status for KSHV, but it would seem that in Uganda other factors are also important in the development of the tumour." .(10).(Risk factors for Kaposi's sarcoma: a case-control study of HIV-seronegative people in Uganda.)
" KS has historically been seen more often in patients whose treatment includes cyclosporine (397), a drug that can reactivate KSHV from latency to lytic replication in tissue culture (225). " .(1).
"Likewise, remission of iatrogenic KS on cessation of immunosuppression is the norm. A recent study in Turkey demonstrated that 8 of 11 iatrogenic KS patients showed complete regression of visceral and cutaneous KS within 6 months of cessation of cyclosporine (141). ". (1).
"We have alluded to the potential for decreases in GSH concentration to impair GSH conjugation and modify the metabolic fate of many compounds. GSH deficiency may contribute to the nephrotoxicity of ischemic events and drug toxicity. This type of toxicity may be exhibited by cyclosporine. Although the exact mechanism of cyclosporine nephrotoxicity remains unknown, its administration has been associated with in vivo reduction of GSH concentrations in the livers and kidneys of rats, which may be related to adverse effects of this immunosuppressive agent.65,66 Cyclosporine has peroxidative properties, induces lipid peroxidation in renal microsomes, and may lead to inactivation of microsomal glucose-6-phosphate activity and toxicity.66,67 Therefore, contribution to cyclosporine nephro- and hepatotoxicity has been postulated to be caused by its generation of free radicals and depletion of GSH. Investigators also have hypothesized that cyclosporine can modify resistance to chemotherapy by augmenting the cytotoxic effect of drugs through inducing a GSH deficiency.65". (11).
"Background. Cyclosporin (CsA) has played an important role in the improvement of solid-organ transplant patients and graft survival. However, nephrotoxicity due to CsA remains an important clinical challenge. The renal toxicity of CsA is attributed to reduced renal blood flow which leads to hypoxia-reoxygenation injury accompanied by excessive generation of oxygen-derived free radicals (ODFR).
N-acetyl-L-cysteine (NAC) is a highly potent antioxidant that has been shown to reduce ODFR injury. In this study an attempt was made to assess the effect of NAC on CsA- induced lipid peroxidation and nephrotoxicity. Methods. Adult Sprague- Dawley rats were treated orally with CsA (25 and 50 mg/kg) alone and in combination with different doses of NAC (10, 20 and 40 mg/kg) for a period of 3 weeks. Twenty-four hours after the last treatment, animals were sacrificed and blood was analysed for blood urea nitrogen (BUN) and serum creatinine (SCr), and kidney samples were analysed for lipid hydroperoxides, conjugated dienes and glutathione, and histopathological changes. Results. Treatment of rats with CsA produced a significant increase in BUN and SCr level and histological abnormalities. CsA-induced impairment of renal toxicity was accompanied by significant increase in renal oxidative stress. NAC treatment significantly protected animals against CsA-induced structural and functional impairment of kidney. Conclusions. CsA-induced nephrotoxicity was significantly attenuated by NAC.
This study clearly suggests the role of oxidative stress in the pathogenesis of CsA-induced nephrotoxicity. Concomitant use of antioxidants such as NAC to minimize CsA-induced nephrotoxicity in humans warrant further studies. Keywords: cyclosporin; free radicals; glutathione; lipid peroxidation; N-acetylcysteine; nephrotoxicity" (4)
"Azathioprine was administered to rats in order to study its interaction with glutathione in vivo. Glutathione levels were measured sequentially in liver, red blood cells, kidney and small intestine after i.p. injections of azathioprine (6.25-100 micronmol/100 g b.wt.). Five minutes after drug administration, dose- related selective depletion of hepatic glutathione up to 50% of control was observed. By 60 minutes 80% depletion of hepatic glutathione was observed. Red cell glutathione depletion was also observed but lagged behind hepatic changes. Five minutes after azathioprine administrations, no change in red cell glutathione was seen with all doses of azathioprine, but a dose-related increase in plasma 6-mercaptopurine and azathioprine was observed. At all azathioprine doses and at all time intervals after drug administration, the hepatic contribution to total glutathione consumption predominated. No change in glutathione levels in kidney or small intestine was observed after azathioprine.
Thus, the liver plays a major role in the metabolism of azathioprine through the interaction of the drug with glutathione.". (17).
"Azathioprine is a myelotoxic and hepatotoxic immunosuppressive agent. Bone marrow and liver are the main targets but gastrointestinal tract, kidney, lungs, CNS and skin may also be affected. Transient gastroenteritis may be observed with massive overdose. Leukopenia is the main toxic effect which may occur during azathioprine therapy and in the overdose patients. Liver and kidney function tests may be altered but usually returned to normal after discontinuation of the drug." .(4).
"Azathioprine is metabolized in vivo to mercaptopurine, apparently by sulphydryl compounds such as glutathione. Mercaptopurine is oxidised and methylated to several derivatives among which 6-thiouric acid predominates; the proportion of metabolites varies amongst individuals. The fate of the nitromethylimidazole portion of azathioprine has not been completely elucidated. Small amounts of azathioprine are also split to give 1-methyl-4-nitro-5-thioimidazole (McEvoy, 1993). The active metabolites, 6-thioguanine nucleotides, responsible for the therapeutic action, are formed intracellularly and appear to have very long half- lives (Maddocks et al., 1986).". (4).
"Azathioprine (AZA) is an important drug used in the therapy of autoimmune system disorders. It induces hepatotoxicity that restricts its use. The rationale behind this study was the proven efficacy of N- acetylcysteine (NAC; a replenisher of sulfhydryls) and reports on the antioxidant potential of aminoguanidine (AG; an iNOS inhibitor), that might be useful to protect against the toxic implications of AZA. AG (100 mg/kg; i.p.) or NAC (100 mg/kg; i.p.) were administered to the Wistar male rats for 7 days and after that AZA (15 mg/kg, i.p.) was given as a single dose. This caused an increase in the activity of hepatic aminotransferases (AST and ALT) in the serum 24 h after AZA treatment. AZA (7.5 or 15 mg/kg, i.p.) also caused an increase in rat liver lipid peroxides and a lowering of reduced glutathione (GSH) contents. In the other part of experiment, protective effects of AG and NAC were observed on AZA induced hepatotoxicity.
NAC significantly protected against the toxic effects produced by AZA. Pretreatment with NAC prevented any change in the activities of both the aminotransferases after AZA. This pretreatment also resulted in a significant decline in the contents of lipid peroxides and a significant elevation in GSH level was evident after AZA treatment.
In the group with AG pretreatment the activities of AST and ALT did not increase significantly after AZA when compared to control. However, the lipid peroxides and GSH levels did not have any significant difference when compared to AZA group. These observations also indicate that the improvement in the GSH levels by NAC is the most significant protective mechanism rather than any other mechanistic profile. The protective effect of AG against the enzyme leakage seems to be through the liver cell membrane permeability restoration and is independent of any effects on liver GSH contents".(18).
"Glutathione is used by the liver to process amyl nitrite, and high glutathione is linked with survival. If using amyl nitrite cuts glutathione, it could lead to disease progression." .(16)
“Two cases are reported of Heinz body haemolytic anaemia [breakdown of red blood cells] after the sniffing of amyl nitrite and butyl nitrite for protracted periods. Nitrites are powerful oxidizing agents which are recognized to cause haemoglobin to be oxidized to methaemoglobin ". (15)
"As early as 1973, patients had presented with unusual symptoms of immune deficiency at London's St Mary's Hospital, all of whom were gay men who used poppers, and all of whom had unprotected anal intercourse (mirroring exactly the first group of gay men who officially gave AIDS its designation a decade later in the US). The inhaled Nitrites (or Nitrates which then convert to Nitrites in the body) combine in blood with the Amines present in faeces to form mutagenic Nitrosamines, the most lethal group of carcinogens known to man. This results in mutations of faecal micro-organisms and viruses and to DNA damage in leukocytes, as well as the formation of Nitrosoglutathione which depletes the body's natural Glutathione defense against toxic chemicals and rugs and against the toxicity of the ubiquitous oxygen radicals. This cascade of immunodestructive events is established today as a causal factor in AIDS." (5)
“Groups of mice were exposed in an inhalation chamber to 900 ppm isobutyl nitrite ['poppers'] for 45 minutes per day for 14 days and then assayed for immune reactivity. The T-dependent antibody responses of nitrite treated mice were reduced by 50-65%…Cytotoxic T cell (CTL) induction was reduced by 40%…and the tumoricidal activity of peritoneal exudate macrophages [cells] was reduced by 40%…[in a later experiment] inhalant exposure increased the tumor incidence from 21% of control mice to 75% of inhalant exposed mice…the rate of increase in mean tumor weight was nearly 4-fold faster in nitrite exposed mice. ” .(6).
"There are important reasons for considering nitrite inhalation as a factor in the development of AIDS-related KS[Kaposi’s Sarcoma] in young male homosexuals. These are (1) the pharmacologic properties of amyl, butyl and isobutyl nitrites, which are toxic; (2) the mutagenic, teratogenic and carcinogenic products resulting from metabolism of N- nitroso compounds; (3) the potent carcinogenicity of N-nitroso compounds in 39 different animal species; and (4) the deleterious effects of volatile nitrites on human lymphocytes both in vitro and in vivo…there are additional reasons for pursuing the connection between nitrite inhalation and development of KS.
These include: (1) the timing of the production and sales of volatile nitrites for use as recreational drugs and the subsequent outbreak of the AIDS epidemic (7 to 10 years); (3) the extensive use of nitrities among male homosexuals; (3) the virtual universal history of nitrite use by young male homosexuals in whom KS has developed during the past 3 years; and (4) the age group in which KS is developing is consistent with a cohort initially exposed 7 to 10 years ago. ” .(12).
“The studies presented here [on mice] show that chronic inhalation of AN [amyl nitrites] can lead to a decrease in helper cells, thus alternting the T-cell H/S [Helper=CD4/Suppressor=CD8] ratio, which is the same phenomenon that occurs in AIDS victims. This suggests a link between AN inhalation and cellular immunity depression. ” .(13).
" 8 HIV-negative male volunteers gave informed consent to participate in this study…Over 4 days of the second week [after obtaining baseline immunologic data], each volunteer participated in 13 [amyl nitrite and placebo] inhalation sessions…the absolute number of blood lymphocytes decreased significantly following the inhalation protocol, then returned to baseline levels…The results showed that exposure to amyl nitrite can induce changes in immune function even after short exposure to moderate doses. ” .(14).
"Although the accumulated evidence suggests a role of decreased GSH in the pathogenesis of HIV, significant controversy remains concerning the mechanism of GSH depletion, especially in regard to envisioning appropriate therapeutic strategies to help compensate for such decreased antioxidant capacity. Tat, a transactivator encoded by HIV, is sufficient to cause GSH depletion in vitro and is implicated in AIDS-associated Kaposi's sarcoma and B cell lymphoma".(7).
"Primary murine embryonic fibroblasts transfected with HIV-1 TAT demonstrated decreased levels of high energy phosphates (ATP, GTP, UTP/CTP), adenine nucleotides (ATP, ADP, AMP), and both NAD+/NADH redox pairs, resulting in a substantial loss of redox poise. A greater than 50% decrease in intracellular reduced glutathione (GSH) concentration was accompanied by the extracellular appearance of acidic fibroblast growth factor (FGF-1). Addition of either N-acetyl-L-cysteine or glutathione ester (GSE), but not L-2-oxothiazolidine 4-carboxylate, partially restored intracellular GSH levels and resulted in loss of extracellular FGF-1. Treatment of FGF-1-transduced cells with buthionine sulfoximine (BSO) resulted in a time- and dose-dependent decrease in total cellular GSH concentration that was accompanied by the extracellular appearance of FGF- 1. Inclusion of GSE during BSO treatment eliminated the extracellular appearance of FGF-1. BSO treatment of cells transfected with a mutant form of FGF-1, in which all three cysteine residues were replaced with serines, also decreased total cellular GSH concentration but failed to induce the extracellular appearance of FGF-1. Collectively, these results suggest that HIV-1 TAT induces a condition of oxidative stress, which mediates cellular secretion of FGF-1, an observation relevant to the pathophysiologic development and progression of AIDS-associated Kaposi's sarcoma."(20)
"It has been found that AIDS is characterised by a persistent oxidative imbalance. An increasing deficiency of the non-toxic anti- oxidant glutathione plays a crucial role in the transition from pre-AIDS to full blown disease (1,2) To quote from Montagnier (the discoverer of HIV) et al ".(21)
"A vicious cycle has been envisaged in which undernourished HIV- infected persons have micronutrient deficiencies, leading to further immunosuppression and oxidative stress and subsequent acceleration of HIV replication and CD4+ T-cell depletion.1 " (22)
"Most importantly, this theory predicts that reducing agents may prevent or even ameliorate KS in homosexual AIDS patients. In this regard, the recent discovery of significant reductions in cellular reduced glutathione in AIDS patients lends strong support for contemplating such a therapeutic strategy [53, 54, 55]." (19)
"The thiol N-acetyl-L-cysteine (NAC), an analogue and precursor of reduced glutathione, has cancer chemopreventive properties attributable to its nucleophilicity, antioxidant activity, and a variety of other mechanisms.
We demonstrated recently that NAC has anti-invasive, antimetastatic, and antiangiogenic effects in in vitro and in vivo test systems. In the present study, s.c. transplantation of KS-Imm cells in (CD-1)BR nude mice resulted in the local growth of Kaposi’s sarcoma, a highly vascularized human tumor. The daily administration of NAC with drinking water, initiated after the tumor mass had become established and detectable, produced a sharp inhibition of tumor growth, with regression of tumors in half of the treated mice along with a markedly prolonged median survival time. The production of vascular endothelial growth factor (VEGF) and certain proliferation markers (proliferating cell nuclear antigen and Ki- 67) were significantly lower in Kaposi’s sarcomas from NAC-treated mice than from control mice. Treatment of KS-Imm cells with NAC in vitro resulted in a dose-dependent inhibition of chemotaxis and invasion through inhibition of gelatinase-A (matrix metalloproteinase-2, MMP-2) activity without altering MMP-2 or MMP-9 mRNA levels.
NAC also significantly inhibited VEGF production but did not affect proliferation markers in vitro. Reverse transcription-PCR analysis indicated that total VEGF mRNAs were reduced by 10 mM NAC. Taken together, these findings provide evidence that NAC, the safety of which even at high doses has been established in almost 40 years of clinical use, in addition to its chemopreventive action, has a strong antiangiogenic potential that could be exploited for preventing cancer progression as well as used in cancer adjuvant therapy." .(8).
and another study looking at other antioxidants this time green tea finds.
"The effects of green tea and EGCG were tested in a highly vascular Kaposi’s sarcoma (KS) tumor model and on endothelial cells in a panel of in vivo and in vitro assays.".(9).
"Results: EGCG inhibited KS-IMM cell growth and endothelial cell growth, chemotaxis, and invasion over a range of doses; high concentrations also induced tumor cell apoptosis. EGCG inhibited the metalloprotease-mediated gelatinolytic activity produced by endothelial cell supernatants and the formation of new capillary-like structures in vitro. Green tea or purified EGCG when administered to mice in the drinking water inhibited angiogenesis in vivo in the Matrigel sponge model and restrained KS tumor growth. Histological analysis of the tumors were consistent with an anti-angiogenic activity of EGCG and green tea." .(9).
"Conclusions: These data suggest that the green tea gallate or its derivatives may find use in the prevention and treatment of vascular tumors in a chemoprevention or adjuvant setting." .(9).
References. (1)MMBR Online
Microbiology and Molecular Biology Reviews, June 2003, p. 175-212, Vol. 67, No. 2 1092-2172/03/$08.00+0 DOI: 10.1128/MMBR.67.2.175-212.2003 Copyright © 2003, American Society for Microbiology. All Rights Reserved.
(2) Journal of Infection Volume 43, Issue 3 , October 2001, Pages 195-199
doi:10.1053/jinf.2001.0899 Copyright © 2001 The British Infection Society. All rights reserved. Regular Article Prevalence, Incidence and Correlates of HHV-8/KSHV Infection and Kaposi's Sarcoma in Renal and Liver Transplant Recipients
(3) Nephrol Dial Transplant (2000) 15: 1443-1445 © 2000 European Renal Association-European Dialysis and Transplant Association Human herpes virus 8 infection in kidney transplant patients in Belgium
Nephrology Dialysis Transplantation, Vol 14, Issue 4 923-929, Copyright © 1999 by Oxford University Press
N-acetylcysteine attenuates cyclosporin-induced nephrotoxicity in rats M Tariq, C Morais, S Sobki, M Sulaiman and A Khader Department of Nephrology and Research Centre, Armed Forces Hospital, W-912 PO Box 7897, Riyadh 11159, Saudi Arabia; Corresponding author
(5)Subject: Poppers article Date: Thu, 12 Oct 1995 01:41:57 -0400 (106 lines of text) From: Facpat at aol.com
Continuum, vol. 3, no. 3, Sept./Oct. 1995, p. 10. http://www.aidsinfobbs.org/articles/quilty/q04/1528
(6)Soderberg LSF. Increased tumor growth in mice exposed to inhaled isobutyl nitrite. Toxicology Letters. 1999 Jan 11;104(1-2):35-41.
(7) J Biol Chem, Vol. 275, Issue 5, 3693-3698, February 4, 2000 Molecular Mechanism of Decreased Glutathione Content in Human Immunodeficiency Virus Type 1 Tat-transgenic Mice*
(8) Cancer Research Clinical Cancer Research Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics Molecular Cancer Research Cell Growth & Differentiation [Cancer Research 61, 8171-8178, November 15, 2001] © 2001 American Association for Cancer Research
(9)Clinical Cancer Research Online Clinical Cancer Research Vol. 10, 4865-4873, July 15, 2004 Experimental Therapeutics, Preclinical Pharmacology Mechanisms of Inhibition of Tumor Angiogenesis and Vascular Tumor Growth by Epigallocatechin-3-Gallate
(10)Int J Cancer. 2003 Jan 10;103(2):233-40. Risk factors for Kaposi's sarcoma: a case-control study of HIV- seronegative people in Uganda http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R etrieve&db=PubMed&list_uids=12455038 &dopt=Abstract (11) The Annals of Pharmacotherapy 1995; 29:1263-73. Reprinted with permission from The Annals of Pharmacotherapy www.theannals.com GLUTATHIONE IN HEALTH AND DISEASE: PHARMACOTHERAPEUTIC ISSUES Ben M Lomaestro and Margaret Malone http://www.redwings.org/HTMLarts/gshhealtha.htm
(12)Newell GR, Spitz MR, Wilson MB. Nitrite Inhalants: Historical Perspective. NIDA Research Monograph. 1988;83:1-14.
13)Ortiz JS, Rivera VL. Altered T-Cell Helper/Suppressor Ratio in Mice Chronically Exposed to Amyl Nitrite. NIDA Research Monograph. 1988;83:59-73.
(14)Dax EM et al. Effects of Nitrites on the Immune System of Humans. NIDA Research Monograph. 1988;83:75-80.
(15)Romeril KR, Concannon AJ. Heinz body haemolytic anaemia after sniffing volatile nitrites. Med J Aust. 1981 Mar 21;1:302-3.
(17)Volume 200, Issue 3, pp. 479-486, 03/01/1977 Copyright © 1977 by American Society for Pharmacology and Experimental Therapeutics Interaction of azathioprine and glutathione in the liver of the rat N Kaplowitz
(18)Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology Volume 134, Issue 4 , April 2003, Pages 451-456 A comparison of hepatoprotective activities of aminoguanidine and N- acetylcysteine in rat against the toxic damage induced by azathioprine M. Raza, , M. Ahmad, A. Gado and O. A. Al-Shabanah
(19) KAPOSI'S SARCOMA AND HIV
Published in Medical Hypotheses Volume 39, pages 22-29, 1992 Eleni Papadopulos-Eleopulos, Valendar F. Turner Department of Medical Physics Emergency Department Royal Perth Hospital email@example.com http://www.sumeria.net/aids/kshiv.html
(20)Arch Biochem Biophys. 1998 Mar 1;351(1):17-26. Glutathione depletion associated with the HIV-1 TAT protein mediates the extracellular appearance of acidic fibroblast growth factor. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?c md=Retrieve&db=PubMed&list_uids=950191 9&dopt=Abstract
(21) Montagnier et al (1997) Oxidative protein damage and degradation in lymphocytes from patients infected with human immunodeficiency virus. Journal of Infectious Diseases 176:655-64
(22) Taken from editorial New England Journal of Medicine July 1 2004. http://content.nejm.org/cgi/content/full/351/1/78#R8
Competing interests: Long term Survivor of hiv/oxidative stress/aids Researcher Continuum Magazine,Member of www.altheal.org , clinnical trials volunteer