The effect of methylmercury on the distribution and excretion of selenium by the guinea pig.

The influence of methylmercury (MeHg) on the tissue and subcellular binding of selenium was determined. Adult female guinea pigs received either 75Se (as sodium selenite) or MeHg (as chloride) followed 5 h later by an equimolar dose of 75Se. Animals were sacrificed 1, 3, 7, and 13 days after administration. Pretreatment with MeHg significantly altered the organ distribution of 75Se, particularly during the first week of the study. 75Se concentrations were markedly reduced in most organs of animals receiving both 75Se and MeHg except the liver, which contained markedly elevated 75Se levels. The subcellular distribution of 75Se was also altered by MeHg. Within liver, kidney and brain, 75Se was primarily bound to nuclear and mitochondrial fractions in both treatment groups, but nuclear binding was higher in animals receiving both compounds. Within nuclear fractions, most 75Se was bound to insoluble-nonhistone proteins. In the presence of MeHg, total nuclear binding of 75Se increased, but total binding to insoluble-nonhistone proteins decreased. MeHg also reduced the total 75Se binding to high molecular weight proteins of the soluble fraction. Alterations in tissue and subcellular binding of MeHg and Se may contribute to the lower degree of toxicity observed in animals receiving both compounds.