Vitamin E and selenium have been recognized as physiological antioxidants in the prevention of oxidative damage to tissues. Rotruck et al. (1) found that selenium was able to help prevent oxidative damage to rat erythrocytes incubated with glucose, as evidenced by decreased hemolysis and decreased hemoglobin oxidation. Vitamin E , however, protected only against hemolysis, whether with or without glucose, but did not prevent hemoglobin oxidation. These results indicated that the effect of selenium was specific and distinct from that of vitamin E. Later, it was demonstrated by Rotruck et al.(2) that selenium was an integral and essential part of glutathione (GSH) peroxidase. Glutathione peroxidase was reported to be responsible for the destruction of lipid peroxides in cells (3,4). Reduced GSH is a hydrogen donor for the GSH peroxidase reaction and is itself regenerated through the reaction of GSH reductase, using NADPH from the oxidation of glucose in the phosphogluconate pathway ( 2 , 3 , 5 ) . Noguchi et al. (6) showed that GSH peroxidase was present mainly in cytosol and the plasma while the action of vitamin E was thought to be primarily within the membrane. A new hypothesis (2, 5 , 6) is now being presented that vitamin E functions by neutralizing the free radicals at the site of their formation whereas GSH peroxide appears to be involved in the intracellular decomposition of lipid hydroperoxides formed. However, the relationship between dietary vitamin E supplementation and activity of GSH peroxidase in tissues has not been thoroughly investigated. The present study was undertaken to investigate the effects of a wide range of dietary vitamin E supplementation (from 0 to 25,000 IU vitamin E/kg diet) on the activity of GSH Supported by the National Research Council of Canada, Grant No. A-4686 and University of British Columbia Research Grant.peroxidase in some tissues, such as the liver, plasma, and uterus of female rats.Materials and methods. Female weanling rats of Wistar strain weighing approximately 50 g were randomly divided into six groups with four rats in each group. Food and water were supplied ad libitum. The basal tocopherol-deficient diet of Draper et al. (7), with supplements of 0, 25, 250, 2500, 10,000, and 25,000 IU vitamin E (df-a-tocopheryl acetate)/kg diet was fed to six groups of rats for 8 months. Blood samples were taken from the inferior vena cava after anesthetizing the animals with ether, and the liver and uterus were removed. The plasma, liver, and uterus were frozen and stored until further analysis. The liver and uterus were minced and then homogenized in 5 vol of KCl (0.124 M ) first with a Sorvall microhomogenizer attached to an omnimixer and then with a motor-driven Potter-Elvehjem homogenizer. The homogenate was subjected with osmotic shock to facilitate release of GSH peroxidase from mitochondria. The activity of GSH peroxidase in diluted homogenate of liver, uterus, and diluted plasma was determined by Mills' procedure 2 (8) with the modification of Hafeman et al. (9). The pr...

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