Mercurys neurotoxicity is characterized by its disruption of selenium biochemistry
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Mercurys neurotoxicity is characterized by its disruption of selenium biochemistry

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  • Journal Title:
    Biochimica et Biophysica Acta (BBA) - General Subjects
  • Personal Author:
  • NOAA Program & Office:
    NMFS (National Marine Fisheries Service)
  • Description:
    Background: 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.

    Scope of review: This focused review examined research literature regarding distinctive characteristics of CH3Hg+ toxicity to identify Se-dependent aspects of its biochemical mechanisms and effects.

    Conclusions: 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 vulnerability, and latency. This review reconsiders the concept that Se is a “tonic” that protects against CH3Hg+ toxicity and recognizes Se's role as Hg's molecular “target”. As the most potent intracellular nucleophile, the selenoenzyme inhibition paradigm has broad implications in toxicology, including resolution of conundrums of CH3Hg+ toxicity.

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  • Source:
    Biochimica et Biophysica Acta (BBA) - General Subjects, 1862(11): 2405-2416
  • DOI:
  • Document Type:
    Journal Article
  • Funding:
    Grant no. NA09NMF4520172
  • Rights Information:
    Accepted Manuscript
  • Compliance:
    CHORUS
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