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Selenium and mercury poisoning
Identifier
006296
Type of Spiritual Experience
Background
Two papers
A description of the experience
Ecotoxicol Environ Saf. 1991 Jun;21(3):348-64. Mercury and selenium interaction: a review. Cuvin-Aralar ML, Furness RW. Binangonan Freshwater Station, Southeast Asian Fisheries Development, Center Aquaculture Department, Rizal, Philippines.
This paper reviews studies on mercury and selenium interaction. It includes the effects of selenium on mercury toxicity on the organism, organ/tissue, and subcellular levels. The paper also touches on possible mechanisms for the "protective action" of selenium against mercury toxicity and deals briefly with the synergism between the two elements.
PMID: 1868791
Toxicology. 2010 Nov 28;278(1):112-23. doi: 10.1016/j.tox.2010.06.004. Epub 2010 Jun 16. Dietary selenium's protective effects against methylmercury toxicity. Ralston NV, Raymond LJ. Energy & Environmental Research Center, University of North Dakota, 15 North 23rd Street, Grand Forks, ND 58202, USA. nralston@undeerc.org
Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity.
Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets.
Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms.
It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues. Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity. Because Hg's binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis.
This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm. However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern. Further studies of these relationships are needed to assist regulatory agencies in protecting and improving child health.
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
PMID: 20561558