| Abstrakt: |
The ability of vitamin E (dl-α-tocopheryl acetate) to protect against methyl mercury toxicity in the rat was tested and the mechanism by which protection might occur was investigated. Increasing dietary vitamin E from 50 to 500 ppm increased growth and survival and decreased toxicity signs in rats poisoned with 10 to 30 ppm Hg as CH3HgCl in the drinking water. This protective effect was shown in rats fed various levels of Se, as well as in rats depleted of Se. Poisoning with CH3HgCl caused an elevation in plasma tocopherol level, that was only partially explained by an elevation in plasma lipids. Tocopherol levels in brain, testes, or liver were not influenced by CH3HgCl poisoning. The antioxidant N,N′-diphenyl-p-phenylenediamine (DPPD) was more effective than vitamin E in protecting Se-depleted rats against CH3HgCl toxicity. When DPPD was added to the diet, the mercury concentration decreased in the whole body, brain and liver, but increased in the kidney. DPPD also altered the distribution of total mercury in the body; smaller proportions were found in the brain, lung and testes, whereas greater proportions were found in the kidney, skin and hair. The form of mercury present in the tissues was not affected by DPPD. The results demonstrated that vitamin E and DPPD protect against CH3HgCl toxicity by a mechanism that is independent of the Se status of the rat and which may involve altered tissue distribution and/or elimination of the mercury. |
