In:
American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 284, No. 3 ( 2003-03-01), p. G536-G545
Abstract:
The objective of this study was to define the relationship among Kupffer cells, O[Formula: see text]production, and TNF-α expression in the pathophysiology of postischemic 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-α, and NADPH oxidase-deficient mice, we found that 45 or 90 min of partial (70%) liver ischemia and 6 h of reperfusion (I/R) produced time-dependent increases in liver injury and TNF-α expression in the absence of neutrophil infiltration. Furthermore, we observed that hepatocellular injury induced by short periods of ischemia were not dependent on formation of TNF-α but were dependent on Kupffer cells and NADPH oxidase-independent production of O[Formula: see text] . However, liver injury induced by extended periods of ischemia appeared to require the presence of Kupffer cells, NADPH oxidase-derived O[Formula: see text], and TNF-α expression. We conclude that the sources for O[Formula: see text] formation and the relative importance of TNF-α in the pathophysiology of I/R-induced hepatocellular injury differ depending on the duration of ischemia.
Type of Medium:
Online Resource
ISSN:
0193-1857
,
1522-1547
DOI:
10.1152/ajpgi.00400.2002
Language:
English
Publisher:
American Physiological Society
Publication Date:
2003
detail.hit.zdb_id:
1477329-6
SSG:
12
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