Effect of chronic ethanol consumption on activation of nitrosopyrrolidine to a mutagen by rat upper alimentary tract, lung, and hepatic tissue.

Tissues derived from male Sprague-Dawley rats which had been pair-fed isocaloric ethanol or carbohydrate control diets for 4 weeks were used to determine the effect of chronic ethanol exposure on the activation of the smoking and diet-associated procarcinogen nitrosopyrrolidine (NPY). Microsomal preparations from lungs and liver and S9 fractions from alimentary tract mucosa were tested for their capacity to activate NPY to a mutagen by the Ames Salmonella assay. Chronic ethanol exposure resulted in an increased capacity to activate NPY by microsomes derived from liver, lungs, and esophagus but not from stomach. The three tissues in which enhanced activation of NPY was observed in the present study also have been noted in epidemiological studies to be target sites of alcohol abuse-associated increased cancer risk. The results presented here suggest that dietary ethanol's effect on carcinogen metabolism may be responsible, at least in part, for the increased cancer risk observed in chronic alcohol abusers.