Effects of sodium chloride and ethanol on stomach tumorigenesis in ACI rats treated with N-methyl-N'-nitro-N-nitrosoguanidine: a quantitative morphometric approach.

Abstract

Effects of sodium chloride (NaCl) and ethanol on gastric tumor development in rats after treatment with N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) were studied. MNNG, dissolved in distilled water (5 g/liter), was administered orally once fay gastric tube at a dose of 0.25 ml/10 g body weight to 4‐week‐old ACI rats. After this carcinogen initiation, animals were fed on a diet containing 10% NaCl (Group 2) or normal diet with 10% ethanol in the drinking water (Group 4). MNNG alone (Group 1), NaCl alone (Group 3), ethanol alone (Group 5), and control (Group 6) animals were also maintained. All survivors were killed one year after the MNNG application. Incidences of tumors in the forestomach and glandular stomach were significantly increased in Group 2 as compared to Group 1 (P<0.05). The height of the pyloric mucosa was significantly greater in Group 2 than in Groups 4, 5 or 6 (P<0.05). In the fundic area, the mucosal height was significantly decreased in Group 4 as compared to Group 6 (P< 0.05). The present results demonstrate that whereas tumors in the glandular stomach and forestomach are both promoted by NaCl, ethanol is without influence. Furthermore, NaCl, a promoter of glandular stomach tumorigenesis also increases cell proliferation.