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Selenium detoxification by methylation

B S Hassoun1, I S Palmer, C Dwivedi

  • 1Station Biochemistry, South Dakota State University, Brookings 57007, USA.

Research Communications in Molecular Pathology and Pharmacology
|October 1, 1995
PubMed
Summary
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Selenium detoxification primarily occurs through methylation. This study investigated methyltransferase activity in rat liver, finding variations between strains and linking methylation to selenium

Area of Science:

  • Biochemistry
  • Toxicology
  • Environmental Health

Background:

  • Methylation is the primary detoxification pathway for selenium.
  • Transmethylation, catalyzed by methyltransferases, is key for forming methylated compounds.
  • Understanding methyltransferase activity is crucial for selenium toxicity research.

Purpose of the Study:

  • To assay methyltransferase activity in liver cytosol from different rat strains.
  • To investigate the role of methylation in selenium detoxification and toxicity.
  • To compare selenium volatilization and lethal dose 50 (LD50) across rat strains.

Main Methods:

  • Liver cytosol preparation from Fischer, Wistar, and Sprague-Dawley rats.
  • High-Performance Liquid Chromatography (HPLC) assay to measure epinephrine formation from norepinephrine, indicating methyltransferase activity.

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  • Intraperitoneal injection of selenium (Se) to assess volatilization and determine LD50.

    • Main Results:

    • Methyltransferase activity varied significantly among rat strains: Fischer (1.65 x 10^-12), Wistar (0.74 x 10^-12), and Sprague-Dawley (1.2 x 10^-12) moles epinephrine formed/mg protein/hr.
    • Selenium volatilization was higher in Wistar rats compared to Fischer rats.
    • LD50 values for Wistar and Fischer rats were 2.58 and 3.15 mg Se/kg, respectively.

    Conclusions:

    • Rat strain significantly influences methyltransferase activity and selenium metabolism.
    • Enhanced methylation of dimethyl selenide to trimethyl selenide is likely a critical detoxification mechanism for selenium.
    • Differences in methylation capacity may explain variations in selenium toxicity and tolerance among rat strains.