Dietary Supplements of Vitamin E, β-Carotene, Coenzyme Q10 and Selenium Protect Tissues Against Lipid Peroxidation in Rat Tissue Slices

Abstract

A tissue slice model was employed to assess the effects of dietary antioxidant supplements on lipid peroxidation. In one experiment, rats were fed diets containing, either alone or in combination, vitamin E, selenium, beta-carotene or coenzyme Q10 for 42 d, and the extent of spontaneous and induced lipid peroxidation was determined by release of thiobarbituric acid-reactive substances (TBARS) into the medium. Vitamin E exhibited the greatest protection against lipid peroxidation in liver, heart and spleen; in kidney, selenium was most protective. Coenzyme Q10 was active against lipid peroxidation induced by tertbutyl hydroperoxide (t-BHP). In a second experiment, rats were fed diets containing varying amounts of vitamin E, selenium, beta-carotene and coenzyme Q10 for 30 d. Spontaneous lipid peroxidation in liver, kidney and heart decreased with increasing levels of dietary antioxidants. With increasing amounts of antioxidants, there was a diminution in TBARS released by liver and kidney slices incubated with t-BHP; in heart, only the highest levels of antioxidants significantly decreased production of TBARS. Inverse correlations between dietary vitamin E and TBARS, tissue vitamin E and TBARS, and tissue selenium-glutathione peroxidase and TBARS were highly significant. The procedure used here can evaluate dietary supplements that may find practical applications in decreasing the oxidant radical portion of disease processes.

Recovery after dietary vitamin E supplementation of impaired endothelial function in vitamin E‐deficient rats

“…It is thought to act by trapping lipid peroxy radical (L0OO) and lipid (L) radical species, thus breaking the lipid peroxidation chain (Burton et al, 1982;1983). Vitamin E has been shown to protect animal tissues against oxidative damage, such as lipid peroxidation, both in vitro and in vivo (Tappel, 1980;Leibovitz et al, 1990) and it is now accepted that vitamin E has physiological and pharmacological roles in certain disorders. Neural tissues appear to be particularly susceptible to a deficiency of vitamin E probably because neuronal cells have a special vulnerability to oxidative injury and subsequently a special need for antioxidant to protect their lipid membranes (Harding, 1987;Muller & Goss-Sampson, 1989;.…”

Exercise and oxidative stress: Sources of free radicals and their impact on antioxidant systems

“…Reduced ubiquinone acts as an antioxidant in vitro and its role as an antioxidant in vivo has been proposed (94). Tissue slices from rats fed a high-ubiquinone diet demonstrated more resistance to hydroperoxide-induced lipid peroxidatJon than those from rats fed a control diet (95). These antioxidative properties have prompted several studies using dietary supplementation of Qlo to evaluate its protective function during exercise.…”

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

“…Antioxidant defense is achieved by additive or synergistic action of enzymes and antiox-idant nutrients (11,12). Selenium and vitamin E in particular appear to have overlapping and partly compensative functions (13)(14)(15)(16)(17). Therefore, it is conceivable that the relation between selenium status and risk of coronary heart disease is influenced by the status of other antioxidants, as has been observed in an animal experiment (18).…”