Biological Trace Element Research

, 133:83

Selenium Supplementation Decreases Hepatic Fibrosis in Mice After Chronic Carbon Tetrachloride Administration

  • Ming Ding
  • James J. Potter
  • Xiaopu Liu
  • Michael S. Torbenson
  • Esteban Mezey
Article

DOI: 10.1007/s12011-009-8414-x

Cite this article as:
Ding, M., Potter, J.J., Liu, X. et al. Biol Trace Elem Res (2010) 133: 83. doi:10.1007/s12011-009-8414-x

Abstract

Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl4-induced liver injury and fibrosis. Mice were administered CCl4 over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl4. Se decreased liver inflammation but not necrosis caused by CCl4. Se increased hepatocyte apoptosis after CCl4 and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl4 in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl4. Liver matrix metalloproteinase-9 increased after CCl4 with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl4 in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.

Keywords

SeleniumStellate cellsCollagenMetalloproteinasesCaspasesApoptosis

Copyright information

© Humana Press Inc. 2009

Authors and Affiliations

  • Ming Ding
    • 1
  • James J. Potter
    • 1
  • Xiaopu Liu
    • 1
  • Michael S. Torbenson
    • 2
  • Esteban Mezey
    • 1
    • 3
  1. 1.Department of MedicineThe Johns Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of PathologyThe Johns Hopkins University School of MedicineBaltimoreUSA
  3. 3.The Johns Hopkins University School of MedicineBaltimoreUSA