Abstract
Summary The mechanisms involved in the protection of selenite against the toxicity of HgCl 2 were investigated with rats. Pretreatment with Se was found to increase markedly the Hg content in the blood and testis, while significantly decreasing that in the kidney. The Hg content in the liver was increased slightly by Se. However, the Hg in the soluble fraction, a major subcellular Hg-binding component, was markedly diverted from low molecular weight proteins to large molecular weight ones in the liver, testis and kidney. Although less pronounced, the diversion also occurred in the plasma. Thus, we propose that Se counteracts Hg toxicity by altering tissue concentration of this element and by diverting tissue Hg to presumably less critical components, similar to the way it counteracts Cd toxicity.
Published Version
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