Effect of selenium on methylmercury binding to subcellular and soluble proteins in rat tissues.

The possible mechanism involved in the protection of Se against the toxicity of methylmercury was investigated with rats. Pretreatment with Se increased the Hg content slightly in the blood (30%), moderately in the testes (doubled), and markedly in the brain (5 times), while decreasing that in the kidneys by half. The Hg content in the liver, spleen, heart and plasma was not significantly affected. Of the subcellular fractions, most (40-50%) of the tissue Hg was found in the soluble fraction (cytosol) of the liver, kidneys and spleen, but not the brain which had 65% of its Hg located in the crude nuclear fraction and only 24% in the soluble fraction. Se did not significantly affect the subcellular Hg distribution other than that which could be accounted for by its effect on the whole tissue uptake. In the soluble fraction, most of the Hg was associated with hemoglobin-containing and low molecular weight (MW less than 5,000) fractions, which is in contrast to reported data for inorganic Hg which binds to metallothionein (MW = 10,000). The distribution pattern of methylmercury between different molecular weight proteins within the soluble fraction was not significantly affected by Se which is also in contrast to reported work on inorganic Hg. Thus, Se pretreatment may protect the kidneys by reducing their methylmercury uptake, but apparently protects other organs by a different mechanism. The possible mechanism of protection by Se against inorganic Hg in which this element is diverted to presumably less critical proteins in the soluble fraction is apparently not operating in the case of methylmercury.