Intestinal mucosal alterations in experimental cirrhosis in the rat: Role of oxygen free radicals
Article first published online: 30 DEC 2003
Copyright © 2002 American Association for the Study of Liver Diseases
Volume 35, Issue 3, pages 622–629, March 2002
How to Cite
Ramachandran, A., Prabhu, R., Thomas, S., Reddy, J. B., Pulimood, A. and Balasubramanian, K. A. (2002), Intestinal mucosal alterations in experimental cirrhosis in the rat: Role of oxygen free radicals. Hepatology, 35: 622–629. doi: 10.1053/jhep.2002.31656
- Issue published online: 30 DEC 2003
- Article first published online: 30 DEC 2003
- Manuscript Accepted: 5 DEC 2001
- Manuscript Received: 21 AUG 2001
- Wellcome Trust, London
- Council of Scientific and Industrial Research, Government of India to A.R., R.P., and S.T.
Cirrhosis is associated with altered gastrointestinal function, and bacterial translocation from the gut plays an important role in the etiology of spontaneous bacterial peritonitis (SBP) seen in this condition. Although alterations in gut motility and intestinal permeability are recognized in cirrhosis, the intestinal damage at the cellular and subcellular levels is not well understood. This study looked at the mucosal alterations in experimental cirrhosis and the role of oxygen free radicals in this process. It was shown that cirrhosis results in oxidative stress in the intestine, as seen by increased xanthine oxidase (XO) activity and altered antioxidant status. Cirrhosis also affects enterocyte mitochondrial function, as assessed by respiratory control ratio, swelling, and calcium flux. Increased lipid peroxidation of the brush border membranes (BBMs) was seen along with altered intestinal transport. In conclusion, this study shows that intestinal mucosal alterations are seen in experimental cirrhosis and are possibly mediated by oxidative stress.