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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.
Summary
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.
- 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.