A role of selenium against methylmercury toxicity

Abstract

SINCE Parizek et al.¹ reported that administration of selenite clearly decreased toxicity of mercuric chloride, there have been many studies on the mechanisms responsible for the interrelationship between selenium and inorganic or organic mercury. Almost all have shown that inorganic selenium, especially selenite, prevents growth inhibition as well as mortality and neurotoxicity due to methylmercury given simultaneously in the diet of Japanese quail^2–4 and rats^5–8. Protective effects of selenium against methylmercury toxicity do not involve mercury absorption through intestines⁹ or excretion in the urine and faeces⁶. Selenite does not increase the rate of breakdown of methylmercury⁷, and thionein does not have a significant role in the detoxification of methylmercury³, but presumably, the form of methylmercury is modified in some way by selenium. We present here evidence that selenite can release methylmercury from its linkage with proteins and thereby influence its tissue distribution.