Literature DB >> 8727253

Aldehyde dehydrogenases of the rat colon: comparison with other tissues of the alimentary tract and the liver.

T Koivisto1, M Salaspuro.   

Abstract

Intracolonic bacteria have previously been shown to produce substantial amounts of acetaldehyde during ethanol oxidation, and it has been suggested that this acetaldehyde might be associated with alcohol-related colonic disorders, as well as other alcohol-induced organ injuries. The capacity of colonic mucosa to remove this bacterial acetaldehyde by aldehyde dehydrogenase (ALDH) is, however, poorly known. We therefore measured ALDH activities and determined ALDH isoenzyme profiles from different subcellular fractions of rat colonic mucosa. For comparison, hepatic, gastric, and small intestinal samples were studied similarly. Alcohol dehydrogenase (ADH) activities were also measured from all of these tissues. Rat colonic mucosa was found to possess detectable amounts of ALDH activity with both micromolar and millimolar acetaldehyde concentrations and in all subcellular fractions. The ALDH activities of colonic mucosa were, however, generally low when compared with the liver and stomach, and they also tended to be lower than in small intestine. Mitochondrial low K(m) ALDH2 and cytosolic ALDH with low K(m) for acetaldehyde were expressed in the colonic mucosa, whereas some cytosolic high K(m) isoenzymes found in the small intestine and stomach were not detectable in colonic samples. Cytosolic ADH activity corresponded well to ALDH activity in different tissues: in colonic mucosa, it was approximately 6 times lower than in the liver and about one-half of gastric ADH activity. ALDH activity of the colonic mucosa should, thus, be sufficient for the removal of acetaldehyde produced by colonic mucosal ADH during ethanol oxidation. It may, however, be insufficient for the removal of the acetaldehyde produced by intracolonic bacteria. This may lead to the accumulation of acetaldehyde in the colon and colonic mucosa after ingestion of ethanol that might, at least after chronic heavy alcohol consumption, contribute to the development of alcohol-related colonic morbidity, diarrhea, and cancer.

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Year:  1996        PMID: 8727253     DOI: 10.1111/j.1530-0277.1996.tb01091.x

Source DB:  PubMed          Journal:  Alcohol Clin Exp Res        ISSN: 0145-6008            Impact factor:   3.455


  18 in total

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2.  The activity of class I, III, and IV of alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in gastric cancer.

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3.  Systemic Adeno-Associated Virus-Mediated Gene Therapy Prevents the Multiorgan Disorders Associated with Aldehyde Dehydrogenase 2 Deficiency and Chronic Ethanol Ingestion.

Authors:  Yuki Matsumura; Na Li; Hanan Alwaseem; Odelya E Pagovich; Ronald G Crystal; Matthew B Greenblatt; Katie M Stiles
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5.  ERK is involved in EGF-mediated protection of tight junctions, but not adherens junctions, in acetaldehyde-treated Caco-2 cell monolayers.

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7.  The diagnostic value of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) measurement in the sera of colorectal cancer patients.

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Journal:  Dig Dis Sci       Date:  2010-01-13       Impact factor: 3.199

Review 8.  Alcoholic pancreatitis: A tale of spirits and bacteria.

Authors:  Alain Vonlaufen; Laurent Spahr; Minoti V Apte; Jean-Louis Frossard
Journal:  World J Gastrointest Pathophysiol       Date:  2014-05-15

9.  The activity of class I, II, III, and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in colorectal cancer.

Authors:  Wojciech Jelski; Bogdan Zalewski; Lech Chrostek; Maciej Szmitkowski
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10.  Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with colorectal cancer.

Authors:  W Jelski; B Zalewski; L Chrostek; M Szmitkowski
Journal:  Clin Exp Med       Date:  2008-01-11       Impact factor: 3.984

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