Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/21117
Full metadata record
DC FieldValueLanguage
dc.contributor.authorBarbouti, A.en
dc.contributor.authorAmorgianiotis, C.en
dc.contributor.authorKolettas, E.en
dc.contributor.authorKanavaros, P.en
dc.contributor.authorGalaris, D.en
dc.date.accessioned2015-11-24T19:12:48Z-
dc.date.available2015-11-24T19:12:48Z-
dc.identifier.issn0891-5849-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21117-
dc.rightsDefault Licence-
dc.subjectApoptosis/*drug effectsen
dc.subjectApoptosomes/metabolismen
dc.subjectCaspase 9/*antagonists & inhibitors/metabolismen
dc.subjectCysteine/metabolismen
dc.subjectCytochromes c/metabolismen
dc.subjectEnzyme Activation/drug effectsen
dc.subjectHumansen
dc.subjectHydrogen Peroxide/*pharmacologyen
dc.subjectIron/*metabolismen
dc.subjectJurkat Cellsen
dc.subjectOxidation-Reductionen
dc.titleHydrogen peroxide inhibits caspase-dependent apoptosis by inactivating procaspase-9 in an iron-dependent manneren
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.freeradbiomed.2007.06.020-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17936184-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0891584907004480/1-s2.0-S0891584907004480-main.pdf?_tid=98d64aee6abe01e67c1c8bd509fd8e28&acdnat=1333090378_38433625bb9620c5db927dacb9b5e458-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2007-
heal.abstractApoptosis represents a physiological form of cell death, the perturbation of which may contribute to the development of several diseases connected with accumulation of unwanted cells or excessive cell loss. We have previously shown that the continuous presence of low concentrations of H2O2 (generated by the action of glucose oxidase) was able to inhibit caspase-mediated apoptosis in Jurkat cells. The main purpose of the present study was to elucidate the exact molecular mechanism(s) underlying this inhibitory action of H2O2. The results presented show that events like outer mitochondrial membrane permeabilization, release of cytochrome c from mitochondria, oligomerization of Apaf-1, and recruitment of procaspase-9 to apoptosomes were taking place normally, but further advancement toward activation of the execution caspases was interrupted when H2O2 was present during the apoptotic process. From the results presented in this work, it emerges that the inhibition of procaspase-9 autoactivation was probably due to the reversible oxidation of sensitive cysteine residues in this molecule. Remarkably, caspase-9 activation and the ensuing caspase cascade proceeded normally in the presence of H2O2 under conditions of iron deprivation, indicating that the inhibition of procaspase-9 activation was an iron-dependent process. Collectively, these results highlighted the potential role of available intracellular iron ions in signaling mechanisms related to apoptotic cell death.en
heal.journalNameFree Radic Biol Meden
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

Files in This Item:
File Description SizeFormat 
Barbouti-2007-Hydrogen peroxide in.pdf1.21 MBAdobe PDFView/Open    Request a copy


This item is licensed under a Creative Commons License Creative Commons