1-METHYL-4-PHENYLPYRIDINIUM HAS GREATER NEUROTOXIC EFFECT AFTER SELENIUM DEFICIENCY THAN AFTER VITAMIN-E-DEFICIENCY IN RAT STRIATUM

The present study was designed to assess the extent of the protective effect of antioxidative capacity of dopaminergic neurons against the p ossible oxidative stress produced by 1-methyl-4-phenylpyridinium. We h ave studied the direct effect of 1-methyl-4-phenylpyridinium on striat um slices from rats fed with selenium-deficient or vitamin E-deficient diets for 30 days. Glutathione peroxidase activity decreased signific antly 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 acid and 3-methoxytyramin e in animals with both restriction diets was higher than in controls. However, this effect was significantly greater in animals with low sel enium diets than with vitamin E-deficient diets in terms of dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid, which were all s ignificantly more depleted by 1-methyl-4-phenylpyridinium in selenium- deficient rats than in vitamin E-deficient rats. Therefore, considerin g changes in the levels of dopamine and its metabolites as an index of 1-methyl-4-phenylpyridinium toxicity, our results seem to indicate th at the glutathione-glutathione peroxidase system has a greater protect or effect than vitamin E.