Natarajan, Sathish Kumar ; Basivireddy, Jayasree ; Ramachandran, Anup ; Thomas, Simmy ; Ramamoorthy, Prabhu ; Pulimood, Anna B. ; Jacob, Molly ; Balasubramanian, Kunissery A. (2006) Renal damage in experimentally-induced cirrhosis in rats: role of oxygen free radicals Hepatology, 43 (6). pp. 1248-1256. ISSN 0270-9139
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Official URL: http://www3.interscience.wiley.com/journal/1126368...
Related URL: http://dx.doi.org/10.1002/hep.21179
Abstract
Cirrhosis with ascites is associated with impaired renal function accompanied by sodium and water retention. Although it has been suggested that mediators such as nitric oxide play a role in the development of renal failure in this situation, other mechanisms underlying the process are not well understood. This study examined the role of oxidative stress in mediating renal damage during the development of cirrhosis in order to understand mechanisms involved in the process. It was shown that carbon tetrachloride- or thioacetamide-induced cirrhosis in rats results in oxidative stress in the kidney as seen by increased lipid peroxidation and protein oxidation, accompanied by altered antioxidant status. Cirrhosis was also found to affect renal mitochondrial function, as assessed by measurement of the respiratory control ratio, the swelling of mitochondria, and calcium flux across mitochondrial membranes. Increased lipid peroxidation and changes in lipid composition were evident in the renal brush border membranes, with compromised transport of 14C glucose across these membranes. In conclusion, renal alterations produced as a result of cirrhosis in the rat are possibly mediated by oxidative stress.
Item Type: | Article |
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Source: | Copyright of this article belongs to American Association for the Study of Liver Diseases. |
ID Code: | 1414 |
Deposited On: | 05 Oct 2010 12:29 |
Last Modified: | 16 May 2016 12:32 |
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