Vitamin E supplementation in the mitigation of carbon tetrachloride induced oxidative stress in rats

Oxidative stress is implicated in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, cataracts and accelerated aging. The aim of this study was to elucidate the protective role of vitamin E supplementation when oxidative stress is induced by CCl4 administration, using the rat as a model. Rats were fed diets for four weeks either with or without dl-α-tocopherol acetate supplementation. Half of the rats (n = 9) from each of the diet groups were then challenged with CCl4 at the completion of the four week diet period. Plasma levels of 8-iso-PGF2α, antioxidant micronutrients and antioxidant enzyme activities were measured to examine changes in oxidative stress subsequent to the supplementation of dl-α-tocopherol in the diet. Plasma α-tocopherol (vitamin E) concentrations were higher for the groups supplemented with dl-α-tocopherol acetate, however the supplemented diet group that was subsequently challenged with CCl4 had significantly lower (p <0.001) plasma α-tocopherol concentration than the dl-α-tocopherol acetate diet group that was not challenged with CCL4. Total plasma 8-iso-PGF2α concentration was elevated in diet groups challenged with CCl4, however, the concentration was significantly lower (p <0.001) when the diet was supplemented with dl-α-tocopherol acetate. The antioxidant enzymes were not influenced by either dietary α-tocopherol manipulation or by the inducement of oxidative stress with CCl4. Plasma concentrations of trans-retinol (vitamin A) were reduced by CCl4 administration in both the dl-α-tocopherol acetate supplemented and unsupplemented diet groups. The results of this study indicate that dl-α-tocopherol acetate supplementation was protective of lipid peroxidation when oxidative stress is induced by a pro-oxidant challenge such as CCl4.