Modification of methylmercury toxicity and metabolism by selenium and vitamin E: possible mechanisms

Abstract

Selenium and vitamin E exert powerful effects in reducing acute or chronic methylmercury toxicity. Levels of selenium normally found in foods (below 1 ppm) delay the onset of toxic signs caused by much higher levels of methylmercury. Tissue levels of mercury in selenium-supplemented animals equal or exceed those found in animals given methylmercury alone. Selenium does not appear to act by simply modifying intake, absorption, excretion, or distribution of methylmercury, and direct effects of both selenium and vitamin E have been observed in vitro when methylmercury was added to cultured nervous tissue cells. The only established functions for selenium and vitamin E in animals are related to the prevention of oxidative damage in tissues. To encompass the protective effects of selenium and vitamin E and to explain other toxicological aspects of methylmercury and other alkylmetals, a new hypothesis is proposed: The toxicity of the alkylmetals is not caused soley by the intact molecule, but also involves free radicals formed by homolytic fission of the carbon-metal bond.