Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22222
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dc.contributor.authorGalaris, D.en
dc.contributor.authorToft, E.en
dc.contributor.authorRydstrom, J.en
dc.date.accessioned2015-11-24T19:22:59Z-
dc.date.available2015-11-24T19:22:59Z-
dc.identifier.issn8755-0199-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22222-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectAnimals, Newbornen
dc.subjectCells, Cultureden
dc.subjectDaunorubicin/*toxicityen
dc.subjectGlutathione/*metabolismen
dc.subjectHeart/*drug effectsen
dc.subjectMyocardium/metabolismen
dc.subjectRatsen
dc.titleEffect of daunorubicin on subcellular pools of glutathione in cultured heart cells from neonatal ratsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/3215553-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1988-
heal.abstractAlterations in cellular GSH and its compartmentation were investigated as a possible mechanism of toxicity of the anthracycline derivative daunorubicin in neonatal heart cells. Cultured beating heart cells from neonatal rats were exposed to daunorubicin at therapeutically relevant concentrations and the resulting changes in cellular GSH as well as cytosolic and mitochondrial pools of GSH were determined. Toxicity was estimated as an increased permeability of the plasma membrane to cytosolic enzymes, e.g., lactate dehydrogenase. Control heart cells were found to contain 12.2 +/- 1.8 nmoles GSH/10(6) cells. Daunorubicin caused a rapid initial decrease followed by a transient increase in cellular GSH. The extent of the latter increase was dependent on the concentration of daunorubicin. High concentrations of daunorubicin gave only a slight increase followed by a pronounced decrease in cellular GSH. By applying a digitonin-based method the effect of daunorubicin on the cytosolic and mitochondrial pools of GSH were separated. The concentration of cytosolic and mitochondrial reduced GSH was estimated to be 8.9 +/- 1.5 nmoles/10(6) cells and 3.3 +/- 0.6 nmoles/10(6) cells, respectively. The results indicate that daunorubicin caused a decrease of cytosolic GSH and, after a short lag period, a release of alctate dehydrogenase. No decrease of mitochondrial GSH occurred under these conditions indicating that daunorubicin influences selectively cytosolic GSH. No lipid peroxidation products were detected in DRB-treated cells under conditions when lactate dehydrogenase was released. Likewise, addition of the iron-chelator desferrioxamin did not influence the release of lactate dehydrogenase, whereas dithiothreitol offered partial protection.(ABSTRACT TRUNCATED AT 250 WORDS)en
heal.journalNameFree Radic Res Communen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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