Stimulation of chemically induced rectal carcinogenesis by chronic ethanol ingestion.

The effect of chronic ethanol administration on 1, 2-dimethylhydrazine-induced rectal carcinogenesis was investigated in 32 paired male Sprague-Dawley rats fed a nutritionally-adequate liquid diet containing 36% of the total calories as either ethanol or isocaloric carbohydrates. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs 6; P less than 0.02), whereas no cocarcinogenic effect of ethanol was observed in other parts of the intestine. Alcohol did not influence tumor size or histopathology. A 47% increase in the activity of mucosal alcohol dehydrogenase in the distal colorectal region was found between chronically-ethanol-fed rats and pair-fed controls (0.241 +/- 0.019 vs 0.164 +/- 0.020 mumol/mg of protein/hr; P less than 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Faecal bile acids, however, do not play a role as promotors of rectal carcinogenesis under the present experimental conditions. The results give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.