High Dietary Intake of Vitamin E Causes Lowered Total Plasma Oxidation In Hypercholesterolemic Rats

Abstract

Oxidative stress appears to play a key role in the development of atherosclerosis. Patients with cardio-vascular diseases have increased plasma lipid peroxides. Low-density lipoprotein cholesterol (LDL) in plasma must undergo oxidative modification before giving rise to foam cells, one of the earliest stages in the development of atherosclerosis. Epidemiological evidence suggests that high dietary intake of vitamin E may protect plasma from oxidation, thereby reducing the risk for heart disease. To test this hypothesis, five groups of hypercholesterolemic rats were fed diets containing various amounts of vitamin E, ranging from zero milligrams (deficient diet) to 2400 milligrams (high level supplementation). Total plasma oxidation was determined by measuring the formation of malondialdehyde (a lipid peroxidation product) at baseline and after inducing iron-catalyzed lipid peroxidation. The results are summarized below: Vitamin E Malondialdehyde formation (mg/kg diet) (nmol/ml plasma) Baseline Oxidation Group I 60 3.636 5.395 Group II 0 6.673 23.197 Group III 300 8.252 22.358 Group IV 600 7.532 15.864 Group V 2400 8.392 13.896 (Group I - no cholesterol control diet) KEY FINDINGS: Upon iron-induced oxidation, MDA formation from baseline values was highest in the animals that were vitamin E deficient (group II). The formation of MDA decreased steadily from baseline values as vitamin E levels went higher. Decreased MDA formation in group I could be due to the low cholesterol substrate levels available for oxidation. It appears that high levels of vitamin E supplementation may exert a protective effect by decreasing lipid peroxidation, thereby reducing the oxidative stress.