[The change of certain biochemical indexes and apotosis protein (Fas/FasL) expression in rat liver of selenium and iodine deficiency]

Wei Sheng Yan Jiu. 2008 Nov;37(6):682-4.
[Article in Chinese]

Abstract

Objective: To investigate the effect of selenium (Se) and iodine (I) deficiency on certain biochemical indexes and apotosis protein (Fas/FasL) expression.

Method: Healthy SD rats were divided into 4 groups at random, including control group, Se deficient group, I deficient group and both Se and I deficient group.The rats in each group were given different man-made feeds containing different levels of Se and I to breed. The second generation rats were chosen as research subjects. The GPX-Px activity and MDA and NO contents and expression of apoptosis protein (Fas/FasL) in liver were determined by chromometry and western blot.

Result: GPX-Px of rat liver in Se deficient group significantly reduced, MDA and NO content s and expression of apoptosis of Fas/FasL increased. There were no apparent change in GPX-Px activities and NO contents of rat liver in I deficient group, while the contents of MDA and Fas/FasL expressions were much higher. The changes of GSH-Px activities and contents of MDA, NO as well as the Fas/FasL expressions in both Se and I deficiency groups are much higher than those of Selenium and Iodine deficiency groups.

Conclusion: Se deficiency can cause the decrease of GPX-Px activities of rat liver and the increase of contents of MDA and NO. It can also lead to over expression of Fas/FasL. It seems that I deficiency can enhance the effect of selenium deficiency.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Fas Ligand Protein / genetics
  • Fas Ligand Protein / metabolism*
  • Female
  • Glutathione Peroxidase / metabolism
  • Iodine / deficiency*
  • Liver / metabolism*
  • Liver / pathology
  • Male
  • Malondialdehyde / metabolism
  • Nitric Oxide / metabolism
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Selenium / deficiency*
  • fas Receptor / genetics
  • fas Receptor / metabolism*

Substances

  • Fas Ligand Protein
  • Faslg protein, rat
  • fas Receptor
  • Nitric Oxide
  • Malondialdehyde
  • Iodine
  • Glutathione Peroxidase
  • Selenium