Inhibition of gastric cell proliferation by acetaldehyde
| Autor: | T. Matysiak‐Budnik, Päivi Kärkkäinen, Taina Methuen, Risto O. Roine, Mikko Salaspuro |
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| Rok vydání: | 1995 |
| Předmět: |
Male
Cell Acetaldehyde Biology Pathology and Forensic Medicine Immunoenzyme Techniques 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine In vivo medicine Gastric mucosa Animals Rats Wistar 030304 developmental biology 0303 health sciences Ethanol Dose-Response Relationship Drug Helicobacter pylori Cell growth Stomach Molecular biology 3. Good health Rats medicine.anatomical_structure Biochemistry chemistry Bromodeoxyuridine Cell culture Gastric Mucosa 030211 gastroenterology & hepatology Cell Division |
| Zdroj: | The Journal of pathology. 177(3) |
| ISSN: | 0022-3417 |
| Popis: | Helicobacter pylori possesses alcohol dehydrogenase activity and is capable of producing acetaldehyde from ethanol in vitro. Acetaldehyde is a toxic and reactive compound and has been shown to inhibit the proliferation of many different cell lines in vitro. To study the effects of acetaldehyde on the proliferation of gastric epithelial cells in vivo, we employed an immunohistochemical method after labelling proliferating cells with 5'-bromo-2'-deoxyuridine in rats receiving acetaldehyde intragastrically. Chronic (16 weeks) exposure of gastric mucosa to acetaldehyde given to rats in their drinking water in concentrations of 10 or 20 mM resulted in significant (P < 0.05) inhibition of gastric epithelial cell proliferation, expressed as 332 +/- 36, 348 +/- 8, and 695 +/- 15 proliferating cells per ten high-power (x 400) fields in the groups drinking 10 mM acetaldehyde, 20 mM acetaldehyde, and in controls respectively. In an acute study, significant inhibition of proliferation was observed after as few as 4 days of exposure to acetaldehyde, but only when a higher dose (50 mM) of acetaldehyde was given (438 +/- 44 versus 615 +/- 19 in controls, P < 0.05). The inhibition of gastric cell renewal by acetaldehyde may play a role in the pathogenesis of ethanol- and/or H. pylori-associated gastric diseases by inhibiting normal gastric mucosal protection and repair. |
| Databáze: | OpenAIRE |
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