Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration

Ming Ding, James J. Potter, Xiaopu Liu, Michael Torbenson, Esteban Mezey

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl 4-induced liver injury and fibrosis. Mice were administered CCl 4 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.

Original languageEnglish (US)
Pages (from-to)83-97
Number of pages15
JournalBiological Trace Element Research
Volume133
Issue number1
DOIs
StatePublished - Jan 1 2010
Externally publishedYes

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Keywords

  • Apoptosis
  • Caspases
  • Collagen
  • Metalloproteinases
  • Selenium
  • Stellate cells

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Clinical Biochemistry
  • Inorganic Chemistry
  • Biochemistry, medical

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