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© 1996 Medical Council on Alcohol

research-article

PREVENTION OF ETHANOL-INDUCED CHANGES IN REACTIVE OXYGEN PARAMETERS BY {alpha}-TOCOPHEROL

STEPHEN C. BONDY*, SHIRLEY X. GUO and JAMES D. ADAMS1

Department of Community and Environmental Medicine, Irvine Occupational Health Center, University of California Irvine, Irvine, CA 92717-1825, USA
1Department of Molecular Pharmacology and Toxicology, University of Southern California Los Angeles, CA 90033, USA

*Author to whom correspondence should be addressed

Received 14 November 1995; first review notified 1 March 1996; accepted 12 March 1996

Rats were given a 200 mg/kg body weight daily dose of {alpha}-tocopherol by i.p. injection for 15 days. This resulted in elevated levels of glutathione in both liver and brain, and in a reduced hepatic rate of generation of reactive oxygen species. The depression of hepatic and cerebral glutathione levels in ethanol-consuming rats was prevented by simultaneous treatment with {alpha}-tocopherol. Other putative indices of hepatic pro-oxidant events, namely levels of mixed function oxidase and proteolytic activity, were elevated by {alpha}-tocopherol both in the presence and absence of ethanol In addition, levels of enzymes especially susceptible to oxidative degradation, glutamine synthetase and creatine kinase, were depressed in the liver following treatment with ethanol or {alpha}-tocopherol. Parameters rapidly responsive to oxidative changes revealed the antioxidant property of {alpha}-tocopherol, while protein-based indices reflecting more extended events suggested a pro-oxidant effect of this vitamin. Results suggest that high levels of {alpha}-tocopherol can simultaneously lead to a more reduced intracellular environment and yet to localized evidence of enhanced oxidative events.


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