ATTENUATION BY METHIONINE OF MONOCHLORAMINE-ENHANCED GASTRIC CARCINOGENESIS INDUCED BY N-METHYL-N'-NITRO-N-NITROSOGUANIDINE IN WISTAR RATS

Helicobacter pylori appears to play a major role in the development of gastric cancer in humans. The mechanism behind the carcinogenic or co -carcinogenic effects of H. pylori has not been established, Ammonia, generated by urea from H. pylori, has been studied as a possible cause , However, the ammonia-monochloramine system has been shown to play a more important role in H. pylori-associated mucosal injury, Therefore, the effects of combined administration of monochloramine and methioni ne, singly or together, on the development of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in in bred Wistar rats. After receiving oral MNNC and regular chow pellet fo r 25 weeks, rats received regular chow pellets or chow pellets contain ing 20% ammonium acetate, and normal tap water or water containing 30 mM sodium hypochlorite, with or with out a subcutaneous injection of m ethionine, until the end of the experiment (week 52). Treatment with b oth ammonium acetate and sodium hypochlorite, which produce monochlora mine, significantly increased the incidence of gastric cancers in week 52, whereas the concomitant administration of methionine with ammoniu m acetate and sodium hypochlorite significantly attenuated such enhanc ed gastric carcinogenesis, Spectrophotometric examination revealed tha t methionine scavenged monochloramine, Our findings suggest that H. py lori-associated gastric carcinogenesis may be mediated by monochlorami ne. (C) 1998 Wiley-Liss, Inc.