Faculty Collaboration Database

Hepatocellular oxidant stress following intestinal ischemia-reperfusion injury. J Surg Res 1991 Dec;51(6):467-71 PMID: 1943082

Pubmed ID

1943082

Abstract

Reperfusion of ischemic intestine results in acute liver dysfunction characterized by hepatocellular enzyme release into plasma, reduction in bile flow rate, and neutrophil sequestration within the liver. The pathophysiology underlying this acute hepatic injury is unknown. This study was undertaken to determine whether oxidants are associated with the hepatic injury and to determine the relative value of several indirect methods of assessing oxidant exposure in vivo. Rats were subjected to a standardized intestinal ischemia-reperfusion injury. Hepatic tissue was assayed for lipid peroxidation products and oxidized and reduced glutathione. There was no change in hepatic tissue total glutathione following intestinal ischemia-reperfusion injury. Oxidized glutathione (GSSG) increased significantly following 30 and 60 min of reperfusion. There was no increase in any of the products of lipid peroxidation associated with this injury. An increase in GSSG within hepatic tissue during intestinal reperfusion suggests exposure of hepatocytes to an oxidant stress. The lack of a significant increase in products of lipid peroxidation suggests that the oxidant stress is of insufficient magnitude to result in irreversible injury to hepatocyte cell membranes. These data also suggest that the measurement of tissue GSSG may be a more sensitive indicator of oxidant stress than measurement of products of lipid peroxidation.

Author List

Turnage RH, Bagnasco J, Berger J, Guice KS, Oldham KT, Hinshaw DB

Author

Keith T. Oldham MD Professor in the Surgery department at Medical College of Wisconsin

Scopus

2-s2.0-0026327286   47 Citations

MESH terms used to index this publication - Major topics in bold

Animals
Glutathione
Glutathione Disulfide
Intestines
Ischemia
Lipid Peroxides
Liver
Male
Oxidants
Rats
Reperfusion Injury