Alcohol Metabolism inHelicobacter pylori-infected Stomach
| Autor: | Risto O. Roine, Katja S. Salmela, Mikko Salaspuro |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
medicine.medical_specialty
Alcohol Acetaldehyde Helicobacter Infections Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine Gastric mucosa Animals Humans Ethanol metabolism 030304 developmental biology Alcohol dehydrogenase 0303 health sciences Ethanol Helicobacter pylori biology Stomach Alcohol Dehydrogenase General Medicine biology.organism_classification 3. Good health Endocrinology medicine.anatomical_structure Biochemistry chemistry Gastric Mucosa Gastritis biology.protein 030211 gastroenterology & hepatology |
| Zdroj: | Annals of Medicine. 27:583-588 |
| ISSN: | 1365-2060 0785-3890 |
| DOI: | 10.3109/07853899509002473 |
| Popis: | Studies in our laboratory have revealed that Helicobacter pylori exhibits significant cytosolic alcohol dehydrogenase activity and that the enzyme is fully active at ethanol concentrations prevailing in the stomach during alcohol consumption or after alcohol is completely absorbed from the stomach and is available through blood circulation only. Moreover, even the low levels of endogenous ethanol found in the stomach can be oxidized to acetaldehyde by H. pylori alcohol dehydrogenase. The metabolic significance of the enzyme remains as yet unresolved. Under microaerobic conditions, however, the enzyme could be of importance in the energy metabolism of the organism. In the presence of excess ethanol, H. pylori alcohol dehydrogenase produces significant amounts of acetaldehyde. Acetaldehyde is a toxic and reactive compound and could theoretically be a pathogenetic factor in H. pylori-associated gastric injury. Preliminary studies have indicated that acetaldehyde inhibits gastric mucosal regeneration and forms stable adducts with mucosal proteins. Both of these mechanisms could cause gastric injury. The role of H. pylori-related acetaldehyde formation in vivo, however, needs to be established in future studies. In antral human gastric mucosa, H. pylori infection is associated with a significant decrease in alcohol dehydrogenase activity. Similarly, in specific pathogen-free mice with a prolonged infection, gastric alcohol dehydrogenase activity is decreased; however, this is not clearly reflected in the bioavailability of ethanol or the amount of its first pass metabolism. |
| Databáze: | OpenAIRE |
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