Protective effect of selenium on aluminium-induced oxidative stress in mouse liver in vivo

Environ Toxicol Pharmacol. 2011 Mar;31(2):302-6. doi: 10.1016/j.etap.2010.11.008. Epub 2010 Nov 27.

Abstract

The aim of the study was to evaluate possible protective effects of selenium (Se) against systemic aluminium (Al) toxicity and the redox status of mouse liver after short-term (16 h) exposure to Al in vivo. BALB/c mice were injected i.p. with AlCl(3) (25mg Al(3+) per kg of body mass) or/and Na(2)SeO(3) (1.25mg Se per kg of body mass). The 4-fold increased activity of ALT in serum showed systemic hepatotoxicity that Se could not prevent by competitive mechanisms. The protective effects of Se could only be observed on intracellular oxidative stress events as determined by glutathione status. Exposure to Al leads to the decrease in the total glutathione (GSH(tot)) and GSH/GSSG redox ratio to about 50% of the control. Upon co-exposure to Se+Al, the concentration of GSH(tot) and the redox ratio was restored to the control values. Our results indicate that Se did not have a protective effect on Al-linked liver toxicity, but did ameliorate intracellular oxidative stress processes mediated by glutathione.

MeSH terms

  • Alanine Transaminase / blood
  • Aluminum / toxicity*
  • Animals
  • Antioxidants / pharmacology*
  • Glutathione / metabolism
  • Glutathione Disulfide / metabolism
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Oxidative Stress / drug effects*
  • Selenium / pharmacology*

Substances

  • Antioxidants
  • Aluminum
  • Alanine Transaminase
  • Glutathione
  • Selenium
  • Glutathione Disulfide