Glutathione Level in Mice Brain After Testosterone Administration
Glutathione (GSH), an SH containing tripeptide, is a powerful antioxidant protecting against free radical damage (Meister and Anderson, 1983). Glutathione has a role in the inactivation of a number of drugs and in the metabolic processing of certain endogenous compounds, such as estrogen, prostaglandins and leukotrienes. Such inhibitors and other compounds that increase GSH synthesis, make it possible to effectively manipulate the metabolism of this compound. GSH is also a coenzyme for several enzymes (Meister, 1984). Since GSH serves effectively in the detoxication of many drugs, the GSH status of an animal is of importance in protection against toxicity. Munthe et.al. (1981) reported that the erythrocyte GSH level increased in RA (Rheumatoid Arthritis) patients receiving “2nd line drugs”. This increase is suggested to precede clinical improvement, and is thus potentially a unique biochemical parameter for monitoring therapy. Recently, Igarashi et.al. (1984) reported that hepatic glutathione S-transferase activity is enhanced significantly in rats after testosterone administration. Since little information is available concerning the behaviour of GSH in the mouse brain after testosterone administration, we examined this effect.
KeywordsNeuronal Ceroid Lipofuscinosis Subacute Sclerosing Panencephalitis Testosterone Propionate Testosterone Administration Central Nervous System Oxygen Toxicity
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