Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/21972
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dc.contributor.authorDoulias, P. T.en
dc.contributor.authorChristoforidis, S.en
dc.contributor.authorBrunk, U. T.en
dc.contributor.authorGalaris, D.en
dc.date.accessioned2015-11-24T19:19:36Z-
dc.date.available2015-11-24T19:19:36Z-
dc.identifier.issn0891-5849-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21972-
dc.rightsDefault Licence-
dc.subjectCell Cycle/*drug effects/physiologyen
dc.subjectCell Division/drug effectsen
dc.subjectDNA Damage/*drug effects/physiologyen
dc.subjectDeferoxamine/*pharmacologyen
dc.subjectDynamins/genetics/metabolismen
dc.subjectEndosomes/*drug effectsen
dc.subjectHeLa Cellsen
dc.subjectHumansen
dc.subjectHydrogen Peroxide/*adverse effectsen
dc.subjectIron/deficiency/metabolismen
dc.subjectIron Chelating Agents/pharmacologyen
dc.subjectLysosomes/*drug effectsen
dc.subjectMutationen
dc.subjectTime Factorsen
dc.subjectrab5 GTP-Binding Proteins/genetics/metabolismen
dc.titleEndosomal and lysosomal effects of desferrioxamine: protection of HeLa cells from hydrogen peroxide-induced DNA damage and induction of cell-cycle arresten
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/14583336-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0891584903003964/1-s2.0-S0891584903003964-main.pdf?_tid=0079fefc3b6783a17cc9b49d5477f54a&acdnat=1332404444_2ad47ea03e6d8be3b22f992777121ef5-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2003-
heal.abstractThe role of endosomal/lysosomal redox-active iron in H2O2-induced nuclear DNA damage as well as in cell proliferation was examined using the iron chelator desferrioxamine (DFO). Transient transfections of HeLa cells with vectors encoding dominant proteins involved in the regulation of various routes of endocytosis (dynamin and Rab5) were used to show that DFO (a potent and rather specific iron chelator) enters cells by fluid-phase endocytosis and exerts its effects by chelating redox-active iron present in the endosomal/lysosomal compartment. Endocytosed DFO effectively protected cells against H2O2-induced DNA damage, indicating the importance of endosomal/lysosomal redox-active iron in these processes. Moreover, exposure of cells to DFO in a range of concentrations (0.1 to 100 microM) inhibited cell proliferation in a fluid-phase endocytosis-dependent manner. Flow cytometric analysis of cells exposed to 100 microM DFO for 24 h showed that the cell cycle was transiently interrupted at the G2/M phase, while treatment for 48 h led to permanent cell arrest. Collectively, the above results clearly indicate that DFO has to be endocytosed by the fluid-phase pathway to protect cells against H2O2-induced DNA damage. Moreover, chelation of iron in the endosomal/lysosomal cell compartment leads to cell cycle interruption, indicating that all cellular labile iron is propagated through this compartment before its anabolic use is possible.en
heal.journalNameFree Radic Biol Meden
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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