Mercury's neurotoxicity is characterized by its disruption of selenium biochemistry

Biochimica Et Biophysica Acta. General Subjects
Nicholas V C Ralston, Laura J Raymond

Abstract

Methylmercury (CH3Hg+) toxicity is characterized by challenging conundrums: 1) "selenium (Se)-protective" effects, 2) undefined biochemical mechanism/s of toxicity, 3) brain-specific oxidative damage, 4) fetal vulnerability, and 5) its latency effect. The "protective effects of Se" against CH3Hg+ toxicity were first recognized >50 years ago, but awareness of Se's vital functions in the brain has transformed understanding of CH3Hg+ biochemical mechanisms. Mercury's affinity for Se is ~1 million times greater than its affinity for sulfur, revealing it as the primary target of CH3Hg+ toxicity. This focused review examined research literature regarding distinctive characteristics of CH3Hg+ toxicity to identify Se-dependent aspects of its biochemical mechanisms and effects. Research indicates that CH3Hg+ irreversibly inhibits the selenoenzymes that normally prevent/reverse oxidative damage in the brain. Unless supplemental Se is provided, consequences increase as CH3Hg+ approaches/exceeds equimolar stoichiometries with Se, thus forming HgSe and inducing a conditioned Se deficiency. As the biochemical target of CH3Hg+ toxicity, Se-physiology provides perspectives on the brain specificity of its oxidative damage, accentuated fetal vul...Continue Reading

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May 21, 2020·Frontiers in Genetics·Cláudia S OliveiraJoão B T Rocha
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