We have recently reported that maternal administration of methylmercury caused a striking increase in the selenium concentration in fetal liver accompanied by a decrease in selenium-dependent glutathione peroxidase (GSH-Px) activity. These changes resulted in the lowered bioavailability of selenium as far as the GSH-Px activity was concerned. The present study demonstrated that maternal administration of methylmercury caused a specific alteration of the form of selenium in fetal liver. Sephadex G-200 gel filtration of liver cytosols revealed an additional major peak of selenium in the fetal livers of mice treated with methylmercury. This peak was not present in the liver, kidney, or placenta of mothers treated with methylmercury.
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