EFFECTS OF VITAMIN-E AND SELENIUM ON ANTIOXIDANT DEFENSE IN RAT-HEART

Heart mitochondria, isolated from rats fed diets deficient or suppleme nted with vitamin E (E) and/or selenium (Se), were subjected to time-c ourse assays of lipid peroxidation stimulated by ascorbate/ADP/Fe3+. M itochondria depleted of alpha-tocopherol (alpha-TH) peroxided rapidly as assessed by formation of thiobarbituric acid reactive substances (T BARS). Formation of TEARS was strongly inhibited in mitochondria from rats fed diets supplemented with E. Selenium deficiency, reduced gluta thione (GSH), glutathione disulfide (GSSG) or GSH + GSSG did not affec t the course of lipid peroxidation in mitochondria from rats supplemen ted or deficient in E. Combined E and Se deficiency resulted in signif icantly lower total (oxidized + reduced) mitochondrial coenzyme Q-9 (C oQ-9) concentration compared with control rats supplemented with dieta ry E and Se. Time-course changes in mitochondrial alpha-TH and total C oQ-9 during oxidizing conditions were minor in + E rats. Total CoQ-9 w as reduced substantially, however, during the course of lipid peroxida tion in mitochondria depleted of alpha-TH. Selenium-dependent glutathi one peroxidase (Se-GSHPx) activity was reduced by approximately 96% in heart cytosol, and to a somewhat lesser extent in mitochondria, by di etary Se deficiency. Non-Se GSHPx activity was not detected in heart c ytosol but was detected in very small amounts in heart mitochondria. G lutathione S-transferase activity of heart cytosol was decreased in E and/or Se deficiency. The results of these experiments indicate that m embrane alpha-TH was most effective in inhibiting lipid peroxidation i n heart mitochondria.