Vitamin E attenuates cold-induced rat liver oxidative damage reducing H2O2 mitochondrial release.

Vitamin E is a major chain-breaking antioxidant which is able to reduce liver oxidative damage without modifying aerobic capacity in T3-treated rats. We investigated whether vitamin E has similar effects in hyperthyroid state induced by cold exposure. Cold exposure increased aerobic capacity and O2 consumption in homogenates and mitochondria and tissue mitochondrial protein content. Vitamin E did not modify aerobic capacity and mitochondrial protein content of cold liver, but increased ADP-stimulated respiration of liver preparations. Succinate-supported H2O2 release rates were increased by cold during basal and stimulated respiration, whereas the pyruvate/malate-supported ones increased only during basal respiration. Vitamin administration to cold-exposed rats decreased H2O2 release rates with both substrates during basal respiration. This effect reduced ROS flow from mitochondria to cytosol, limiting liver oxidative damage. Cold exposure also increased mitochondrial capacity to remove H2O2, which was reduced by vitamin treatment, showing that the antioxidant also lowers H2O2 production rate. The different effects of cold exposure and vitamin treatment on H2O2 generation were also found in the presence of respiration inhibitors. Although this can suggest that the cold and vitamin induce opposite changes in mitochondrial content of autoxidizable electron carriers, it is likely that vitamin effect is due to its capacity to scavenge superoxide radical. Finally, vitamin E reduced mitochondrial oxidative damage and susceptibility to oxidants, and prevented Ca2+-induced swelling elicited by cold. In the whole, our results suggest that vitamin E is able to maintain aerobic capacity and attenuate oxidative stress of hepatic tissue in cold-exposed rats modifying mitochondrial population characteristics.