Background and Study Aims: The mechanism of Helicobacter pylori-induced gastric mucosal injury is unknown, but H. pylori infection is conducive to accumulation in the stomach of monochloramine, a cytotoxic substance. The present study involved morphological investigation of the damaging effects of monochloramine on rat gastric mucosa, using endoscopic observations through a gastric fistula. The study also examined the protective effect of taurine against monochloramine-induced gastric mucosal lesions in rats.
Materials and Methods: The effects of monochloramine in rats were studied by administering the substance via a gastrostomy, which was then used to conduct a series of endoscopic observations. Local blood flow was measured using a laser Doppler method. Histological examination was carried out after 24 hours. Various monochloramine concentrations were used, and some animals were pretreated with taurine, a monochloramine scavenger, via the gastrostomy.
Results: Endoscopically, monochloramine was found to produce hemorrhagic mucosal erosions, mainly in the gastric body, in a time-dependent and concentration-dependent manner. Blood flow was decreased in advance of mucosal erosion. Taurine prevented mucosal injury by 30 mM monochloramine, the highest concentration tested.
Conclusions: Although only the first 24 hours of mucosal injury were observed in the present study, the most likely mechanisms by which monochloramine caused injury to the gastric mucosa appeared to be both oxidative damage and a reduction in blood flow, impairing the mucosal defense mechanism.
References
-
1
Murakami M, Asagoe K, Dekigai H, et al.
Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage.
Dig Dis Sci.
1995;
40
268-273
-
2
Marshall B J, Warren J R.
Unidentified curved bacilli on gastric epithelium in active chronic gastritis.
Lancet.
1983;
i
1273-1275
-
3
Grisham M B, Jefferson M M, Thomas E L.
Chlorination of endogenous amines by isolated neutrophil: ammonia-dependent bacterial, cytotoxic, and cytolytic activities of the chloramines.
J Biol Chem.
1984;
259
10404-10413
-
4
Suzuki M, Asako H, Kubes P, et al.
Neutrophil-derived oxidants promote leukocyte adherence in postcapillary venules.
Microvasc Res.
1991;
42
125-138
-
5
Suzuki M, Miura S, Suematsu M, et al.
Helicobacter pylori-associated ammonia production enhances neutrophil-dependent gastric mucosal injury.
Am J Physiol.
1992;
263
725
-
6
Kato S, Nishiwaki H, Konaka A, et al.
Mucosal ulcerogenic action of monochloramine in rat stomachs.
Dig Dis Sci.
1997;
42
2156-2163
-
7
Stapleton P P, O'Flaherty L, Redmond H P, et al.
Host defense: a role for the amino acid taurine?.
JPEN J Parenter Enteral Nutr.
1998;
22
42-48
-
8
Tsukada H, Sakai M, Uchino H, et al.
Endoscopic observation of rat stomach through gastric fistula (in Japanese).
Nihon Shokaki Naishikyo Gakkai Zasshi/Gastroenterol Endosc.
1983;
25
1643-1649
-
9
Thomas E L, Grisham M B, Jefferson M M.
Preparation and characterization of chloramines.
Methods Enzymol.
1986;
132
569-585
-
10
Murakami M, Saita H, Teramura S, et al.
Gastric ammonia has a potent ulcerogenic action on the rat stomach.
Gastroenterology.
1993;
105
1710-1715
-
11
Rocha G A, Queiroz D MM, Mendes E N, et al.
Helicobacter pylori acute gastritis: histological, endoscopic, clinical, and therapeutic features.
Am J Gastroenterol.
1991;
86
1592-1595
-
12
Paauw J D, Davis A T.
Taurine concentrations in serum of injured patients and age- and sex-matched healthy controls.
Am J Clin Nutr.
1994;
52
657-660
-
13
Vinton N E, Laidlaw S A, Ament M E, et al.
Taurine concentrations in plasma and blood cells of patients undergoing long-term parenteral nutrition.
Am J Clin Nutr.
1986;
44
398-404
M.D. M. Kodama
Dept. of Metabolism and Clinical Nutrition Faculty of Medicine Kyoto University
54, Kawahara-cho, Sakyo-ku
Kyoto City 606-8507
Japan
Phone: + 81-75-751-4244
