, Volume 133, Issue 1, pp 83-97
Date: 02 Jun 2009

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

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


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.

This work was supported by grant AA000626 from the US Public Health Service. Ming Ding, Ph.D. was a postdoctoral fellow on National Research Service Award 2 T32 AA07467 from the National Institute of Alcohol Abuse and Alcoholism (NIH).