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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00482.2001
Submitted on November 12, 2001
Accepted on June 14, 2002
1 Departments of Gastroenterology and Endoscopy, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
2 Toride Ishikai Hospital, Toride, Ibaraki, Japan
3 Department of Biochemstry, Juntendo University, School of Medicine, Bunkyo-ku, Tokyo, Japan
4 Department of Cell Biology and Neuroscience, Oska University, Graduate School of Medicine, Osaka, Osaka, Japan
* To whom correspondence should be addressed. E-mail: ynk-aki{at}md.tsukuba.ac.jp.
Gastric luminal ammonia produced by Helicobacter pylori has been shown to cause gastric mucosal injury. This study was conducted to examine the mechanisms, by which gastric luminal ammonia causes apoptosis of gastric epithelial cells. Monolayers of GSM06 cells, developed from murine gastric surface mucous cells, were cultured in the absence or presence of 10-30 mM NH4Cl at ambient pH 5.0, 6.0, and 7.0. In the presence of luminal NH4Cl, GSM06 cells showed (a) cell shrinkage and nuclear chromatin condensation, (b) DNA fragmentation into oligonucleosomes, (c) leakage of cytochrome c into cytosolic fraction without affecting bax expression, and (d) increases in activity of caspases-3 and -9. These changes were accentuated when the cells were cultured at pH 7.0. In the absence of NH4Cl, none of these changes were detected at any pH examined. These results suggest that gastric luminal ammonia, at concentrations detected in Helicobacter pylori-infected subjects, induces apoptosis of gastric epithelial cells by release of cytochrome c from mitochondria, followed by activation of caspases-9 and -3, especially at higher ambient pH.
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