Vitamin E reduces glucocorticoid-induced oxidative stress in rat skeletal muscle.

Abstract

The purpose of this study was to investigate the effect of vitamin E on oxidative stress in the skeletal muscle of glucocorticoid-treated rats. Male Sprague-Dawley rats (5 weeks of age) were fed a basal diet or a diet supplemented with vitamin E (5,000 mg DL-alpha-tocopheryl acetate/kg diet) for 10 d. The rats of both diet groups received subcutaneous injections of corticosterone (CTC) (0, 25, and 100 mg/kg body weight/d) during the final 4 d. Weights of the extensor digitorum longus and gastrocnemius (GAST) muscles were dose-dependently reduced by CTC. However, the muscle weight losses in rats fed the vitamin E diet were smaller than those in rats fed the basal diet. Protein carbonyl content in the GAST muscle, which was determined as an index of oxidatively modified protein, was increased by 100 mg of CTC, and the increment was significantly (p < 0.01) reduced by vitamin E supplement. Hyperglycemia was induced by 100 mg of CTC, but it was not affected by vitamin E. Lipid peroxide (TBARS) in plasma and in GAST muscle was elevated by 100 mg of CTC, and vitamin E significantly (p < 0.001) suppressed the formation of TBARS in the muscle. The change in TBARS paralleled that in protein carbonyl. These results show that CTC leads to oxidative stress in rat skeletal muscles and that vitamin E has roles in reducing the oxidative stress which causes muscle atrophy.