Effects of vitamin E and selenium on antioxidant defense in rat heart

Abstract

Heart mitochondria, isolated from rats fed diets deficient or supplemented with vitamin E (E) and/or selenium (Se), were subjected to time-course assays of lipid peroxidation stimulated by ascorbate/ADP/Fe 3.. Mitochondria depleted of a-tocopherol (a-TH) peroxided rapidly as assessed by formation of thiobarbituric acid reactive substances (TBARS). Formation of TBARS was strongly inhibited in mitochondria from rats fed diets supplemented with E. Selenium deficiency, reduced glutathione (GSH), glutathione disulfide (GSSG) or GSH + GSSG did not affect the course of lipid peroxidation in mitochondda from rats supplemented or deficient in E. Combined E and Se deficiency resulted in significantly lower total (oxidized + reduced) mitochondrial coenzyme Q-9 (CoQ-9) concentration compared with control rats supplemented with dietary E and Se. Time-course changes in mitochonddal a-TH and total CoQ-9 during oxidizing conditions were minor in +E rats. Total CoQ-9 was reduced substantially, however, during the course of lipid peroxidation in mitochondria depleted of a-TH. Selenium-dependent glutathione peroxidase (Se-GSHPx) activity was reduced by approximately 96% in heart cytosol, and to a somewhat lesser extent in mitochondria, by dietary Se deficiency. Non-Se GSHPx activity was not detected in heart cytosol but was detected in very small amounts in heart mitochondria. Glutathione S-transferase activity of heart cytosol was decreased in E and/or Se deficiency. The results of these experiments indicate that membrane a-TH was most effective in inhibiting lipid peroxidation in heart mitochondria.

Contents and Uptake Rates of Mn, Fe, Co, Zn, and Se in Se-Deficient Rat Liver Cell Fractions

“…In fact, it has been reported that TBARS and other indices of lipid peroxidation increased in SeD animals. 25,26 Our previous finding that the uptake rate of Fe in the liver of SeD rats changed with time 27 would seem to be in conflict with the present study, in which the Fe uptake did not change. Because the liver was not perfused in the previous case, the Fedistribution in residual blood might have affected the results to some extent.…”

Trans-Plasma Membrane Electron Transport in Mammals: Functional Significance in Health and Disease

“…The enzymes involved in the last steps of the biosynthetic pathway are exclusively located in the inner mitochondrial membrane; then, ubiquinone uses the endo-exocytic pathway to distribute among cell membranes moving from and to mitochondria through mitochondria-associated membranes, and reaching the plasma membrane (85). Therefore, changes of ubiquinone concentration in plasma membranes may arise either from biosynthesis or translocation from intracellular reservoirs, such as the endoplasmic reticulum and mitochondria (257). Further, the amount of ubiquinone in membranes is also dependent on dietary vitamin E, selenium, and ubiquinone (162,216).…”

Micronutrients and their supplementation in chronic cardiac failure. An update beyond theoretical perspectives

“…High levels of other antioxidants can only delay but not prevent peroxidative damage if membrane-based vitamin E is deficient [102]. Lower vitamin E levels are found in patients with multiple risk factors for coronary disease suggesting impaired or exhausted antioxidative defense [103].…”