Mercurys neurotoxicity is characterized by its disruption of selenium biochemistry
Advanced Search
Select up to three search categories and corresponding keywords using the fields to the right. Refer to the Help section for more detailed instructions.

Search our Collections & Repository

For very narrow results

When looking for a specific result

Best used for discovery & interchangable words

Recommended to be used in conjunction with other fields

Dates

to

Document Data
Library
People
Clear All
Clear All

For additional assistance using the Custom Query please check out our Help Page

i

Mercurys neurotoxicity is characterized by its disruption of selenium biochemistry

Filetype[PDF-792.14 KB]



Details:

  • Journal Title:
    Biochimica et Biophysica Acta (BBA) - General Subjects
  • Personal Author:
  • NOAA Program & Office:
  • 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.

  • Keywords:
  • Source:
    Biochimica et Biophysica Acta (BBA) - General Subjects, 1862(11): 2405-2416
  • DOI:
  • Document Type:
  • Funding:
  • Rights Information:
    Accepted Manuscript
  • Compliance:
    CHORUS
  • Main Document Checksum:
  • Download URL:
  • File Type:

Supporting Files

  • No Additional Files
More +

You May Also Like

Checkout today's featured content at repository.library.noaa.gov

Version 3.27.1