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A microsomal ethanol oxidizing system (MEOS) is present in the colonic mucosa of the rat. This MEOS metabolizes ethanol to acetaldehyde at the physiological pH of 7.4. Alcohol dehydrogenase or catalase are not involved in the reaction. The Michaelis Menten constant of the reaction is 13.7 +/- 0.3 mM and the maximal velocity is 219 +/- 30 pmoles acetaldehyde/mg microsomal protein X min. Bacterial ethanol metabolism does not contribute to the acetaldehyde production in the colonic MEOS. Chronic ethanol consumption has no effect on colonic MEOS activity. In addition, chronic ethanol ingestion does not affect colonic microsomal NADPH-cytochrome-c-reductase nor benzo(a) pyrene hydroxylase activity.

The oral administration of dietary chenodeoxycholic acid (1%), but not of ursodeoxycholic acid (1%), to male Sprague Dawley rats results in a significant increase in the colonic adenylate cyclase activity without any influence on the colonic cyclic-AMP phosphodiesterase activity. No effect of chronic bile acid feeding on the response of colonic adenylate cyclase to prostaglandin E2 and vasoactive intestinal peptide is observed. These data emphasize a dependence of the cyclic-AMP adenylate cyclase activation on the chemical structure of the bile acid. This may be of pathophysiologic relevance with respect to the frequently observed diarrhea as a side effect of oral chenodeoxycholic, but not ursodeoxycholic acid therapy for cholesterol gallstone dissolution in man.