Helicobacter pylori is not a co-carcinogen in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat gastric carcinogenesis.

Helicobacter pylori was implicated in gastric carcinogenesis through the induction of metaplasia of the gastric mucosa. In this experiment a co-carcinogenic effect of H. pylori on chemically induced gastric carcinogenesis was examined. Wistar WKY male rats received drinking water containing 50 mg/l of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and intragastric administration of 10(6) to 10(8) colony forming unit of H. pylori thrice a week for 40 weeks. Thus, 3 groups were assigned as Group I; MNNG alone, Group II; MNNG + vehicle, and Group III; MNNG + H. pylori (n = 30, each). At autopsy, 9 rats (30%) had 7 glandular stomach and 3 duodenal tumors in Group I, and 10 rats (33%) had 8 glandular stomach and 2 duodenal tumors in Group II, whereas in Group III 4 rats (13%) had 2 glandular stomach and 2 duodenal tumors (chi 2 = 4.257, P < 0.15 for the incidences of glandular stomach tumors among 3 groups). The finding seems to suggest that H. pylori has an ambitendency in the gastritis-metaplasia-carcinogenesis sequence as a promoter for the induction of the predisposing mucosa and as an inhibitor against certain carcinogens.