Chronic alcohol muscle disease is characterized by reduced skeletal muscle mass precipitated by acute reduction in protein synthesis. The pathogenic mechanisms remain obscure, but several lines of evidence suggest that increased oxidative stress occurs in muscle in response to alcohol and this may be associated with impaired α-tocopherol status. Potentially, this implies a therapeutic role for α-tocopherol, especially as we have shown that supplemental α-tocopherol may increase the rate of protein synthesis in normal rats [Reilly, Patel, Peters and Preedy (2000) J. Nutr. 130, 3045–3049]. We investigated the therapeutic effect of α-tocopherol on plantaris muscle protein synthesis in rats treated either acutely, chronically or chronically+acutely with ethanol. Protein synthesis rates were measured with a flooding dose of L-[4-3H]phenylalanine. Protein, RNA and DNA contents were determined by standard laboratory methods. Ethanol caused defined metabolic changes in muscle, including decreased protein, RNA and DNA contents in chronically treated rats. In acute or chronic+acute studies, ethanol suppressed fractional rates of protein synthesis. α-Tocopherol supplementation did not ameliorate the effects of either acute, chronic or chronic+acute alcohol on plantaris muscle protein content or rates of protein synthesis. In control animals (not treated with alcohol), α-tocopherol supplementation decreased muscle protein content owing to increases in protein turnover (both synthesis and degradation). α-Tocopherol supplementation is not protective against the deleterious effects of alcohol on protein metabolism in skeletal muscle.
Chronic α-tocopherol supplementation in rats does not ameliorate either chronic or acute alcohol-induced changes in muscle protein metabolism
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Michael KOLL, Julie A. BEESO, Frank J. KELLY, Ulrich A. SIMANOWSKI, Helmut K. SEITZ, Timothy J. PETERS, Victor R. PREEDY; Chronic α-tocopherol supplementation in rats does not ameliorate either chronic or acute alcohol-induced changes in muscle protein metabolism. Clin Sci (Lond) 1 March 2003; 104 (3): 287–294. doi: https://doi.org/10.1042/cs1040287
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