AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 263: G60-G68, 1992;
0193-1857/92 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jaeschke, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jaeschke, H.

AJP - Gastrointestinal and Liver Physiology, Vol 263, Issue 1 60-G68, Copyright © 1992 by American Physiological Society

ARTICLES

Enhanced sinusoidal glutathione efflux during endotoxin-induced oxidant stress in vivo

H. Jaeschke
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Hepatic release of reduced glutathione (GSH) and its oxidation [glutathione disulfide (GSSG) formation] were investigated in male Fischer rats in vivo after administration of various doses (1-15 mg/kg) of endotoxin (Salmonella enteritidis). Endotoxin dose dependently enhanced basal plasma glutathione (9.64 +/- 0.80 microM) and GSSG (1.08 +/- 0.23 microM GSH equivalents) levels by up to 450 and 1,300%, respectively, 60 min after administration of the highest dose. Determination of arteriovenous differences of plasma glutathione and portal vein blood flow demonstrated an increase of basal sinusoidal glutathione efflux (18 nmol.min-1.g liver wt-1) by 300% 15 min after 5 mg/kg endotoxin. Activation of Kupffer cells by retinol enhanced endotoxin-induced release of GSH and its oxidation severalfold. Endotoxin enhanced plasma levels of catecholamines; however, only an epinephrine-induced not the endotoxin-induced stimulation of hepatic GSH efflux was inhibited by adrenergic blockers. Depletion of serum complement by cobra venom factor pretreatment completely abolished the endotoxin-induced increase of GSH release and enhanced GSSG formation. Zymosan-activated serum (source of C5a) increased GSSG formation and GSH release. It is concluded that endotoxin triggered an extracellular oxidant stress and an increased release of hepatic GSH indirectly through complement activation. Increased sinusoidal efflux of GSH and its extracellular oxidation may act as a local defense mechanism against the potentially deleterious effects of reactive oxygen generated by Kupffer cells during their physiological functions.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
J. S. Gujral, J. A. Hinson, A. Farhood, and H. Jaeschke
NADPH oxidase-derived oxidant stress is critical for neutrophil cytotoxicity during endotoxemia
Am J Physiol Gastrointest Liver Physiol, July 1, 2004; 287(1): G243 - G252.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
C. Zhang, L. M. Walker, J. A. Hinson, and P. R. Mayeux
Oxidant Stress in Rat Liver after Lipopolysaccharide Administration: Effect of Inducible Nitric-Oxide Synthase Inhibition
J. Pharmacol. Exp. Ther., June 1, 2000; 293(3): 968 - 972.
[Abstract] [Full Text]

Home page
 Drug Metab. Dispos.Home page
J. S. Halladay, J.-M. Sauer, and I. G. Sipes
Metabolism and Disposition of [14C]1-Nitronaphthalene in Male Sprague-Dawley Rats
Drug Metab. Dispos., December 1, 1999; 27(12): 1456 - 1465.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online