Abstract
Oxygen-derived free radicals have been reported to be closely involved in the development of tissue injury induced by ischemia-reperfusion in several organs, such as heart, brain, lung, liver, stomach, small intestine, kidney and so on. Ischemia itself causes tissue damage, but further injuries can occur when oxygen is reintroduced to the tissue. Furthermore, lipid peroxidation mediated by free radicals is believed to be one of the important causes of biological membrane destruction and cell damage. It has been reported that Vitamin E exists in the cell membrane of various tissues and functions as a lipid-soluble antioxidant by scavenging oxygen-derived free radicals and terminating free radical chain reaction. In experimental ischemia-reperfusion injury model, vitamin E in the tissue was significantly decreased after ischemia-reperfusion. On the other hand, in Vitamin E-deficient animals, ischemia-reperfusion injury was more severe than in Vitamin E-nondeficient animals. These results indicate that Vitamin E is consumed in the process of lipid peroxidation induced by free radicals in ischemia-reperfusion to prevent the development of tissue damage.
