The mechanism of alcohol intolerance produced by various therapeutic agents

dc.contributor.authorVasiliou, V.en
dc.contributor.authorMalamas, M.en
dc.contributor.authorMarselos, M.en
dc.date.accessioned2015-11-24T19:37:21Z
dc.date.available2015-11-24T19:37:21Z
dc.identifier.issn0001-6683-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24020
dc.rightsDefault Licence-
dc.subjectAlcohol Dehydrogenaseen
dc.subjectAlcohol Deterrents/*pharmacologyen
dc.subjectAlcohol Oxidoreductases/*antagonists & inhibitorsen
dc.subjectAldehyde Dehydrogenase/*antagonists & inhibitorsen
dc.subjectAnimalsen
dc.subjectBrain/enzymologyen
dc.subjectEthanol/*adverse effectsen
dc.subjectKineticsen
dc.subjectLiver/enzymologyen
dc.subjectMaleen
dc.subjectRatsen
dc.subjectRats, Inbred Strainsen
dc.titleThe mechanism of alcohol intolerance produced by various therapeutic agentsen
heal.abstractAccording to clinical reports, several therapeutic agents produce ethanol intolerance, which is often referred as disulfiram reaction. The mechanism of this manifestation was investigated in the Wistar rat, by measuring the alcohol and aldehyde dehydrogenases (ADH, ALDH) of the liver and the brain after subacute administration of chloramphenicol (100 mg/kg X 4, intraperitoneally), chlorpropamide (80 mg/kg X 4, intraperitoneally), disulfiram (150 mg/kg X 4, intraperitoneally), griseofulvin (100 mg/kg X 4, intraperitoneally), isoniazid (200 mg/kg X 4, intraperitoneally), metronidazole (200 mg/kg X 4, intraperitoneally), and procarbazine (100 mg/kg X 4, intraperitoneally). All substances tested decrease the activity of the low-Km ALDH in the brain, with the exception of griseofulvin. The hepatic low-Km enzyme is also inhibited, with the exception of griseofulvin and metronidazole. The high-Km ALDH responds in an inconsistent way, while ADH is not affected at all. The results suggest that the so-called "disulfiram-reaction" is mediated mainly, but not exclusively, by inhibition of the low-Km ALDH.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/2943133-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1111/j.1600-0773.1986.tb00114.x/asset/j.1600-0773.1986.tb00114.x.pdf?v=1&t=h096ig6e&s=c6be7116d4d05ea35dd76206d1ee63cffd16d98c-
heal.journalNameActa Pharmacol Toxicol (Copenh)en
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate1986-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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