Pyruvate reduces anoxic injury and free radical formation in
perfused rat hepatocytes.
Borle, Andr[acute]e B., and Ronald T. Stanko.
Department of Cell Biology and Physiology, Clinical Nutrition
Research Unit of the Gastroenterology Division, Department of
Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA
15261
APStracts 2:0228G, 1995.
The effects of 5 mM pyruvate on anoxic injury, on superoxide (O2 x -)
and hydrogen peroxide (H2O2) generation and on LDH release during
reoxygenation following 2 1/2 h anoxia were studied in perfused rat
hepatocytes. When pyruvate was present during anoxia and
reoxygenation, there was little anoxic injury, and the generation of
free radicals and LDH release during reoxygenation were reduced 50
-60%. When pyruvate was added during reoxygenation, there was no
decrease in O2 x - or LDH release although H2O2 formation was
depressed. Free radical formation and anoxic/reperfusion injury were
significantly reduced when pyruvate was added during the anoxic
period only. Pyruvate reduced the deleterious effects of 10 [mu]M
antimycin A by preventing the increase in O2 x - formation and LDH
release evoked by the inhibitor. These results indicate that pyruvate
protected hepatocytes against anoxic injury and that its protective
action occurred principally during anoxia and not during
reoxygenation. Pyruvate appeared to act at a mitochondrial site since
it reduced the deleterious effects of antimycin A.
Received 5 June 1995; accepted in final form 27 September 1995.
APS Manuscript Number G239-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95