Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18960
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dc.contributor.authorDoulias, P. T.en
dc.contributor.authorNousis, L.en
dc.contributor.authorZhu, B. Z.en
dc.contributor.authorFrei, B.en
dc.contributor.authorGalaris, D.en
dc.date.accessioned2015-11-24T18:55:58Z-
dc.date.available2015-11-24T18:55:58Z-
dc.identifier.issn1071-5762-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18960-
dc.rightsDefault Licence-
dc.subjectApoptosis/*drug effectsen
dc.subjectCells, Cultureden
dc.subject*DNA Damageen
dc.subjectHumansen
dc.subjectHydrogen Peroxide/*antagonists & inhibitors/*pharmacologyen
dc.subjectHydroxyl Radical/antagonists & inhibitors/metabolismen
dc.subjectIron/chemistry/pharmacologyen
dc.subjectIron Chelating Agents/pharmacologyen
dc.subjectJurkat Cellsen
dc.subjectMolecular Structureen
dc.subjectOrganic Chemicals/chemistryen
dc.subjectOxidation-Reductionen
dc.subjectTropolone/analogs & derivatives/*pharmacologyen
dc.subjectWater/chemistryen
dc.titleProtection by tropolones against H2O2-induced DNA damage and apoptosis in cultured Jurkat cellsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1080/10715760400017244-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15763960-
heal.identifier.secondaryhttp://informahealthcare.com/doi/pdfplus/10.1080/10715760400017244-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2005-
heal.abstractTropolones, the naturally occurring compounds responsible for the durability of heartwood of several cupressaceous trees, have been shown to possess both metal chelating and antioxidant properties. However, little is known about the ability of tropolone and its derivatives to protect cultured cells from oxidative stress-mediated damage. In this study, the effect of tropolones on hydrogen peroxide-induced DNA damage and apoptosis was investigated in cultured Jurkat cells. Tropolone, added to the cells 15 min before the addition of glucose oxidase, provided a dose dependent protection against hydrogen peroxide induced DNA damage. The IC50 value observed was about 15 microM for tropolone. Similar dose dependent protection was also observed with three other tropolone derivatives such as trimethylcolchicinic acid, purpurogallin and beta-thujaplicin (the IC50 values were 34, 70 and 74 microM, respectively), but not with colchicine and tetramethyl purpurogallin ester. Hydrogen peroxide-induced apoptosis was also inhibited by tropolone. However, in the absence of exogenous H2O2 but in the presence of non-toxic concentrations of exogenous iron (100 microM Fe3+), tropolone dramatically increased the formation of single strand breaks at molar ratios of tropolone to iron lower than 3 to 1, while, when the ratio increased over 3, no toxicity was observed. In conclusion, the results presented in this study indicate that the protection offered by tropolone against hydrogen peroxide-induced DNA damage and apoptosis was due to formation of a redox-inactive iron complex, while its enhancement of iron-mediated DNA damage at ratios of [tropolone]/[Fe3+] lower than 3, was due to formation of a lipophilic iron complex which facilitates iron transport through cell membrane in a redox-active form.en
heal.journalNameFree Radic Resen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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