Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities.

Oxidative stress induced by chronic ethanol consumption, particularly in aging subjects, has been implicated in the pathophysiology of many neurodegenerative diseases. Antioxidants with polyphenol structures, such as those contained in green tea, given alone for 5 weeks in liquid Lieber de Carli diet followed by administration with ethanol for 4 weeks with ethanol have been investigated as potential therapeutic antioxidant agents in the brain in rats of three ages (2, 12, and 24 months). Ethanol consumption caused age-dependent decreases in brain superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities. In addition, ethanol consumption caused age-dependent decreases in the levels of GSH, selenium, vitamins, E, A and C, and beta-carotene and increases in the levels of oxidized glutathione (GSSG). Changes in the brain's antioxidative ability were accompanied by enhanced oxidative modification of lipids (increases in lipid hydroperoxides, malondialdehyde, and 4-hydroxynonenal levels) and proteins (increases in carbonyl groups and bistyrosine). Reduced risk of oxidative stress and protection of the central nervous system, particularly in young and adult rats, after green tea supplementation were observed. Green tea partially prevented changes in antioxidant enzymatic as well as nonenzymatic parameters induced by ethanol and enhanced by aging. Administration of green tea significantly protects lipids and proteins against oxidative modifications in the brain tissue of young and adult rats. The beneficial effect of green tea can result from the inhibition of free radical chain reactions generated during ethanol-induced oxidative stress and/or from green tea-induced increases in antioxidative abilities made possible by increases in the activity/concentration of endogenous antioxidants.