Title Exercise-induced oxidative stress: glutathione supplementation and

deficiency. Author Sen CK; Atalay M; H=E4nninen O Address Department of Physiology, Faculty of Medicine, University of Kuopio, Finland.Source J Appl Physiol, 77: 5, 1994 Nov, 2177-87

Abstract: Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80-90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.

Title Protection from oxidation enhances the survival of cultured mesencephalic

neurons. Author Colton CA; Pagan F; Snell J; Colton JS; Cummins A; Gilbert DL Address Department of Physiology and Biophysics, Georgetown University Medical School, Washington, DC 20007, USA. Source Exp Neurol, 132: 1, 1995 Mar, 54-61

Abstract Oxidative stress has been linked to the destruction of dopaminergic neurons in the substantia nigra and may be a significant factor ( Hg says, read = mercury ) in both Parkinson's disease and MPTP toxicity. Using primary cultures of embryonic rat mesencephalon and standard immunocytochemical techniques, we have examined the survival of tyrosine hydroxylase-containing (TH+) neurons cultured in the presence of antioxidants and/or in an environment of low oxygen partial pressure. The number of TH+ neurons increased approximately twofold if superoxide dismutase, glutathione peroxidase (GP), or N-acetyl cysteine (NAC) were added to the culture media. Exposure of the neurons to a 5% oxygen environment (38 torr, i.e., 38 mm Hg) also increased the survival of TH+ neurons by about twofold. A dramatic enhancement of survival, however, was seen when NAC was used in combination with the 5% oxygen environment. In this case, the number of TH+ neurons increased fourfold from nontreated controls. Morphological changes were also noted. GP increased the average neurite length while NAC increased the average area of the cell body in the TH+ neuron. These results suggest that manipulation of oxidative conditions by changing the ambient O2 tension or the level of antioxidants promotes survival of TH+ neurons in culture and may have implications for transplantation therapies in Parkinson's disease.

Title Suppression of human immunodeficiency virus expression in chronically

infected monocytic cells by glutathione, glutathione ester, and N-acetylcysteine.

Author Kalebic T; Kinter A; Poli G; Anderson ME; Meister A; Fauci AS Address

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Source Proc Natl Acad Sci U S A, 88: 3, 1991 Feb 1, 986-90

Abstract: The effects of glutathione (GSH), glutathione ester (GSE), and N-acetyl-L-cysteine (NAC) on the induction of human immunodeficiency virus (HIV) expression were investigated in the chronically infected monocytic U1 cell line, a previously described cellular model for HIV latency. U1 cells constitutively express low levels of virus, which can be increased by phorbol 12-myristate 13-acetate (PMA), tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and other inducers. GSH, GSE, and NAC suppressed in a dose-dependent fashion the induction of HIV expression mediated by PMA, TNF-alpha, and IL-6, in the absence of cytotoxic or cytostatic effects. Reverse transcriptase activity, inducible by PMA, TNF-alpha, or IL-6, was decreased by 80-90% after pretreatment with GSH, GSE, or NAC. The induction of total HIV protein synthesis was also decreased appreciably after pretreatment with GSH, GSE, or NAC. The accumulation of HIV mRNA was substantially suppressed after pretreatment with NAC but to a lesser extent after pretreatment with GSH or GSE. Although PMA induces the expression of TNF-alpha in U1 cells, the suppressive effect of GSH, GSE, and NAC on PMA-induced HIV expression in U1 cells was not associated with the inhibition of TNF-alpha expression. The present findings, which elucidate relationships between cellular GSH and HIV expression, suggest that therapy with thiols may be of value in the treatment of HIV infection.

Title: The dental amalgam issue. Author Mats Hanson & Jaro Pleva. Source: A review Experentia 47(1991), Birkhauser Verlag, CH-4010 Switzerland,

Abstract: When the mercury etiology of acrodynia was clarified, the possibility that MS was an adult form of acrodynia and a neuroallergic reaction was considered. Baasch recognised the possibility that amalgam fillings could be the responsible source of mercury. He concluded that the amalgam mercury etiology could explain the known facts about MS. Baasch noted the presence or absence of amalgam fillings in 500 consecutive MS patients in Zurich. All but one (or possibly two) had amalgam fillings. However amalgam fillings are common, so this finding proved nothing. On the other hand there are other sources of mercury. Three cases were described by baasch. Two of these had thier amalgam fillings removed and the patients improved. The third one showed a rapidly developing disease, starting a few months after she got her first amalgam fillings at 19 years of age. When 8 years old she had been treated with mercury for congenital syphilis. (My note - statistically 498/500 is more significant than the authors seem to believe,even allowing for high amalgam percentage in population.)

Also make sure to read these books: Poison in Your Teeth: Mercury Amalgam (Silver) Fillings...Hazardous to Your Health! and Mercury Detoxification by Tom McGuire