Inhibition of MNNG-induced gastroduodenal carcinoma in rats by synchronous application of wine or 11% ethanol.

There are divergent opinions on the effect of ethanol in the carcinogenesis of gastroduodenal tumors. The effect of the synchronous application of 11% ethanol or wine (11% ethanol) and N-methyl-N'-nitro-N-nitrosoguanidine (100 micrograms/ml, MNNG) in a drinking solution on the incidence of gastroduodenal tumors was evaluated. Sixty outbred male Wistar rats were distributed among three groups. The animals drank MNNG and ethanol or wine for six months and consumed the same quantity of MNNG. Then they consumed a normal diet until the 13th month, when the experiment was terminated. The stomach and duodenum were examined histologically. In the stomach, 15 tumors (2 squamous paillomas, 4 squamous carcinomas, 1 sarcoma, and 8 adenocarcinomas) and 4 cases of dysplasia were found; in the duodenum, there were four cases of adenocarcinoma. There were 6 cases of multiple tumors. Incidence of forestomach tumors did not differ among the groups, whereas the incidence of glandular stomach carcinoma and duodenal carcinoma was significantly lower in the groups treated with 11% ethanol or wine than in the control group. MNNG was not inactivated by ethanol in the drinking solutions. We concluded that the inhibitory effect on gastroduodenal carcinogenesis is the result of 11% ethanol ingestion and its protective action on the mucosa and not of the wine's nonethanol components.