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Articles in PresS, published online ahead of print November 20, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00400.2002
Submitted on September 18, 2002
Accepted on November 18, 2002
1 Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA, USA
2 DNAX Research Institute, Palo Alto, CA, USA
3 National Jewish Medical and Research Center, Denver, CO, USA
4 Department of Pediatrics, LSU Health Sciences Center, Shreveport, LA, USA
5 Department of Medicine, LSU Health Sciences Center, Shreveport, LA, USA
6 Webb-Waring Institute, University of Colorado Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: mgrish{at}lsuhsc.edu.
The objective of this study was to define the relationship among Kupffer cells (KCs), superoxide production, and tumor necrosis factor-
(TNF-) expression in the pathophysiology of post-ischemic liver injury following short and long periods of ischemia. Using different forms of superoxide dismutase with varying circulating half-lives, a monoclonal antibody directed against mouse TNF-, and NADPH oxidase deficient mice, we found that 45 or 90 minutes of partial (70%) liver ischemia and 6 hours of reperfusion (I/R) produced time-dependent increases in liver injury and TNF- expression in the absence of neutrophil infiltration. Furthermore, we observed that hepatocellular injury induced by short periods of ischemia were not dependent upon formation of TNF- but were dependent upon KCs and NADPH oxidase-independent production of superoxide. However, liver injury induced by extended periods of ischemia appeared to require KCs, NADPH oxidase-derived superoxide, and TNF- expression. We conclude that the sources for superoxide formation and the relative importance of TNF- in the pathophysiology of I/R-induced hepatocellular injury differ depending upon the duration of ischemia.
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