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Am J Physiol Gastrointest Liver Physiol 281: G173-G181, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 1, G173-G181, July 2001

Scavenging nitric oxide reduces hepatocellular injury after endotoxin challenge

Evan P. Nadler1, Eva C. Dickinson1, Donna Beer-Stolz2, Sean M. Alber2, Simon C. Watkins2, David W. Pratt3, and Henri R. Ford1

1 Department of Surgery, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh 15213; and 2 The Center for Biologic Imaging and 3 Department of Chemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

Sustained upregulation of inducible nitric oxide (NO) synthase in the liver after endotoxin [lipopolysaccharide (LPS)] challenge may result in hepatocellular injury. We hypothesized that administration of a NO scavenger, NOX, may attenuate LPS-induced hepatocellular injury. Sprague-Dawley rats received NOX or saline via subcutaneous osmotic pumps, followed 18 h later by LPS challenge. Hepatocellular injury was assessed using biochemical assays, light, and transmission electron microscopy (TEM). Interleukin (IL)-6 mRNA was measured by RT-PCR. Tumor necrosis factor (TNF)-alpha protein expression was determined by immunohistochemistry. NOX significantly reduced serum levels of ornithine carbamoyltransferase and aspartate aminotransferase. TNF-alpha and IL-6 expression were increased in the livers of saline-treated but not NOX-treated rats. Although there was no difference between groups by light microscopy, TEM revealed obliteration of the space of Disse in saline-treated but not in NOX-treated animals. Electron paramagnetic resonance showed the characteristic mononitrosyl complex in NOX-treated rats. We conclude that NOX reduces hepatocellular injury after endotoxemia. NOX may be useful in the management of hepatic dysfunction secondary to sepsis or other diseases associated with excessive NO production.

inducible nitric oxide synthase; endotoxemia; dithiocarbamate; interleukin-6; ornithine carbamoyltransferase


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