The activities of alcohol dehydrogenase (ADH), catalase, microsomal ethanol-oxidizing system (MEOS) and aldehyde dehydrogenase (ALDH) were measured in gastric, small intestinal, colonic and rectal mucosal samples of rats fed on a liquid alcohol diet for 1 month. In the rectum and large intestine of control animals, the activities of ADH, MEOS and catalase were maximal, whereas the activity of ALDH was minimal. After chronic alcohol intoxication, MEOS activity increased significantly in the stomach. An activation of catalase and MEOS and a decrease of the low-K(M) ALDH activity were observed in the rectum of experimental animals. In rats consuming the alcohol diet, hypertrophy of crypts and an increased number of mitoses were noticed in colonic and rectal mucosa. Acute alcohol intoxication (2 g/kg, intragastrically) produced significantly higher acetaldehyde concentrations in the contents of the large intestine and rectum of rats receiving alcohol chronically compared to controls. Thus, after chronic alcohol intoxication, the large intestine regions showed a greater imbalance between the activities of acetaldehyde-producing and -oxidizing enzymes, which resulted in accumulation of acetaldehyde. This mechanism can account for the local toxicity of ethanol after its chronic consumption, and relates the development of mucosal damage and compensatory hyper-regenerative processes, and possibly carcinogenesis, in the colonic and rectal mucosae of alcoholics to the effects of acetaldehyde.

A correlation between the brain acetaldehyde accumulation, but not catalase levels, and the central effect of ethanol was demonstrated in animals genetically differing in initial sensitivity to the hypnotic effect of ethanol.

A correlation between the brain acetaldehyde accumulation, but not catalase levels, and the central effect of ethanol was demonstrated in animals genetically differing in initial sensitivity to the hypnotic effect of ethanol.