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 272: G328-G334, 1997;
0193-1857/97 $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 LeGrand, T. S.
Right arrow Articles by Aw, T. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by LeGrand, T. S.
Right arrow Articles by Aw, T. Y.

AJP - Gastrointestinal and Liver Physiology, Vol 272, Issue 2 328-G334, Copyright © 1997 by American Physiological Society


ARTICLES

Chronic hypoxia, glutathione-dependent detoxication, and metabolic instability in rat small intestine

T. S. LeGrand and T. Y. Aw
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130, USA.

We previously showed that chronic hypoxia decreases activity of intestinal glutathione (GSH)-dependent enzymes and is associated with a proximal-to-distal gradient of enzyme activity, suggesting reduced detoxication capacity in ileal cells. To assess whether hypoxia affects metabolism of hydroperoxides, jejunal and ileal enterocytes from rats exposed to air (n = 11) or 10% O2 (n = 9) for 10 days were exposed to 300 microM tert-butyl hydroperoxide (t-BH). The initial rate of hydroperoxide metabolism was 50-90% faster in hypoxic enterocytes, but cell killing was enhanced. Metabolism in normoxic, but not hypoxic, cells was enhanced threefold by addition of 10 mM glucose. Hypoxic enterocytes exhibited a higher baseline GSH/GSH disulfide (GSSG) ratio but a larger percent decrease after t-BH exposure. t-BH induced a 35-40% decrease in protein-bound sulfhydryl groups in normoxic and hypoxic enterocytes, but protein-bound sulfhydryl was protected by glucose in normoxic cells only. Metabolic response to substrate load or hydroperoxide challenge was assessed by measurement of cellular O2 consumption. Hypoxia, but not normoxia, increases and decreases O2 consumption on exposure to glucose and oxidant, respectively, suggesting metabolic dysregulation. In summary, prolonged O2 deficiency induces loss of intestinal metabolic integrity that is associated with altered peroxide detoxication activity and mitochondrial respiratory function.


This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
T. S. Legrand and T. Y. Aw
Chronic hypoxia alters glucose utilization during GSH-dependent detoxication in rat small intestine
Am J Physiol Gastrointest Liver Physiol, February 1, 1998; 274(2): G376 - G384.
[Abstract] [Full Text] [PDF]




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