AJP - GI AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 283: G1264-G1275, 2002. First published August 28, 2002; doi:10.1152/ajpgi.00235.2002
0193-1857/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/6/G1264    most recent
00235.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
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 Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nakamura, E.
Right arrow Articles by Hagen, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakamura, E.
Right arrow Articles by Hagen, S. J.
Vol. 283, Issue 6, G1264-G1275, December 2002

Role of glutamine and arginase in protection against ammonia-induced cell death in gastric epithelial cells

Eiji Nakamura and Susan J. Hagen

Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215

Ammonia is a cytotoxic factor produced during Helicobacter pylori infection that may reduce the survival of surface epithelial cells. Here we examine whether ammonia kills cells and whether L-glutamine (L-Gln) protects against cell death by stimulating ammonia detoxification pathways. Cell viability and vacuolation were quantified in rat gastric epithelial (RGM1) cells incubated with ammonium chloride at pH 7.4 in the presence or absence of L-Gln. Incubation of RGM1 cells with ammonium chloride caused a dose-dependent increase in cell death and vacuolation, which were both inhibited by L-Gln. We show that RGM1 cells metabolize ammonia to urea via arginase, a process that is stimulated by L-Gln and results in reduced ammonia cytotoxicity. L-Gln also inhibits the uptake and facilitates the extrusion of ammonia from cells. Blockade of glutamine synthetase did not reduce the survival of RGM1 cells, demonstrating that the conversion of L-glutamate and ammonia to L-Gln is not involved in ammonia detoxification. Thus our data support a role for L-Gln and arginase in protection against ammonia-induced cell death in gastric epithelial cells.

Helicobacter pylori; rat; rat gastric epithelial 1 cells; NH4Cl


This article has been cited by other articles:


Home page
 J. Nutr.Home page
S. J. Hagen, M. Ohtani, J.-R. Zhou, N. S. Taylor, B. H. Rickman, G. L. Blackburn, and J. G. Fox
Inflammation and Foveolar Hyperplasia Are Reduced by Supplemental Dietary Glutamine during Helicobacter pylori Infection in Mice
J. Nutr., May 1, 2009; 139(5): 912 - 918.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. Tashima, S. Zhang, R. Ragasa, E. Nakamura, J. H. Seo, A. Muvaffak, and S. J. Hagen
Hepatocyte growth factor regulates the development of highly pure cultured chief cells from rat stomach by stimulating chief cell proliferation in vitro
Am J Physiol Gastrointest Liver Physiol, February 1, 2009; 296(2): G319 - G329.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
J. Xu, J. Henriksnas, S. Barone, D. Witte, G. E. Shull, J. G. Forte, L. Holm, and M. Soleimani
SLC26A9 is expressed in gastric surface epithelial cells, mediates Cl-/HCO3- exchange, and is inhibited by NH4+ (Report)
Am J Physiol Cell Physiol, August 1, 2005; 289(2): C493 - C505.
[Abstract] [Full Text] [PDF]


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