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Ecohealth. 2008 Dec;5(4):456-9. doi: 10.1007/s10393-008-0204-y. Epub 2009 Feb 6.

Mercury toxicity and the mitigating role of selenium.

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Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii at Manoa, Biomedical Sciences Building, Suite 222, 651 Ilalo Street, Honolulu, 96813 HI, USA.


Mercury is a well-known environmental toxicant, particularly in its most common organic form, methylmercury. Consumption of fish and shellfish that contain methylmercury is a dominant source of mercury exposure in humans and piscivorous wildlife. Considerable efforts have focused on assessment of mercury and its attendant risks in the environment and food sources, including the studies reported in this issue. However, studies of mercury intoxication have frequently failed to consider the protective effects of the essential trace element, selenium. Mercury binds to selenium with extraordinarily high affinity, and high maternal exposures inhibit selenium-dependent enzyme activities in fetal brains. However, increased maternal dietary selenium intakes preserve these enzyme activities, thereby preventing the pathological effects that would otherwise arise in their absence. Recent evidence indicates that assessments of mercury exposure and tissue levels need to consider selenium intakes and tissue distributions in order to provide meaningful risk evaluations.

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