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.

Keywords:

• COLD EXPOSURE
• THYROID HORMONE
• VITAMIN E
• OXIDATIVE DAMAGE
• MUSCLE MITOCHONDRIA
• HYDROGEN PEROXIDE RELEASE