1-Methyl-4-phenylpyridinium has greater neurotoxic effect after selenium deficiency than after vitamin E deficiency in rat striatum.

Abstract

The present study was designed to assess the extent of the protective effect of antioxidative capacity of dopaminergic neurons against the possible oxidative stress produced by 1-methyl-4-phenylpyridinium. We have studied the direct effect of 1-methyl-4-phenylpyridinium on striatum slices from rats fed with selenium-deficient or vitamin E-deficient diets for 30 days. Glutathione peroxidase activity decreased significantly after selenium dietary restriction. Our results showed that the effect of 1-methyl-4-phenylpyridinium on dopamine and its metabolites 3,4-dihydroxyphenylacetic acid, homovanillic homovanillic acid and 3-methoxytyramine in animals with both restriction diets was higher than in controls. However, this effect was significantly greater in animals with low selenium diets than with vitamin E-deficient diets in terms of dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid, which were all significantly more depleted by 1-methyl-4-phenylpyridinium in selenium-deficient rats than in vitamin E-deficient rats. Therefore, considering changes in the levels of dopamine and its metabolites as an index of 1-methyl-4-phenylpyridinium toxicity, our results seem to indicate that the glutathione-glutathione peroxidase system has a greater protector effect than vitamin E.