Many bacteria possess marked alcohol dehydrogenase activity and in the presence of ethanol they produce reactive and toxic acetaldehyde. Acetaldehyde production mediated by microbial alcohol dehydrogenases has been demonstrated in the oropharynx and bronchopulmonary washings. Also the most important gastric pathogen, Helicobacter pylori, and many skin bacteria associating with pathological dermatological conditions, possess alcohol dehydrogenase activity and produce acetaldehyde from ethanol. The most richly colonized site of the human body, however, is the large intestine, and therefore bacterial acetaldehyde production is most important in this organ. Alcohol ingested orally is transported to the colon by blood circulation and, after the distribution phase, intracolonic ethanol levels are equal to those in the blood. In the large bowel ethanol is oxidized by a bacteriocolonic pathway. In this pathway intracolonic ethanol is at first oxidized by bacterial alcohol dehydrogenase to acetaldehyde. Then acetaldehyde is oxidized either by colonic mucosal or bacterial aldehyde dehydrogenase to acetate. Part of intracolonic acetaldehyde may also be absorbed via the portal vein and metabolized in the liver. Bacteriocolonic pathway offers a new explanation for the disappearance of a part of ethanol calories. Due to the low aldehyde dehydrogenase activity of colonic mucosa acetaldehyde accumulates in the colon. Accordingly, during ethanol oxidation highest acetaldehyde levels of the body are found in the colon and not in the liver. High intracolonic acetaldehyde may contribute to the pathogenesis of alcohol-induced diarrhoea. Acetaldehyde has been proven to be a carcinogen in experimental animals. It may therefore contribute to the increased risk of colon polyps and colon cancer found to be associated with heavy alcohol consumption in man. Intracolonic acetaldehyde may also be an important determinant of blood acetaldehyde level and a possible hepatotoxin. In addition to acetaldehyde, gut-derived endotoxin is another potential candidate in the pathogenesis of alcohol-related liver injury.