Vitamin E reduces cold-induced oxidative stress in rat skeletal muscle decreasing mitochondrial H2O2 release and tissue susceptibility to oxidants

Abstract

Vitamin E is able to attenuate rat liver oxidative damage without modifying metabolic response to experimental and functional hyperthyroidism. We investigated whether vitamin E has similar effects in skeletal muscle from rats made hyperthyroid by exposure to low environmental temperature. Vitamin treatment was found to maintain cold-induced increases in aerobic capacity and O2 consumption of homogenates and mitochondria, and muscle content of mitochondrial proteins. Conversely, antioxidant treatment limited oxidative damage of muscle preparations as demonstrated by the reduction in hydroperoxide and protein-bound carbonyl levels and enhancement of tissue reduced glutathione content. Vitamin E protects muscle against oxidative damage not only by a direct action on lipids and proteins component of cellular membranes, but also through a modulation of rates of reactive oxygen species generation by muscle mitochondria. Indeed, during basal and stimulated respiration, succinate-supported H2O2 release rates increased in all cold-exposed rats, but in smaller measure in vitamin-treated rats, whereas pyruvate/malate supported H2O2 release rates were not modified by cold exposure and vitamin E treatment. Finally, it was also found that vitamin E treatment offers further protection to skeletal muscle reducing its susceptibility to oxidative challenge. Overall, our results show that vitamin E preserves high aerobic capacity, reducing the high oxidative damage and susceptibility to oxidants elicited in muscle as a response to cold stress.