Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18443
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dc.contributor.authorNoutsopoulos, D.en
dc.contributor.authorMarkopoulos, G.en
dc.contributor.authorKoliou, M.en
dc.contributor.authorDova, L.en
dc.contributor.authorVartholomatos, G.en
dc.contributor.authorKolettas, E.en
dc.contributor.authorTzavaras, T.en
dc.date.accessioned2015-11-24T18:52:51Z-
dc.date.available2015-11-24T18:52:51Z-
dc.identifier.issn1089-8638-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18443-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectBlotting, Northernen
dc.subjectBlotting, Westernen
dc.subjectCell Line, Transformeden
dc.subject*Cell Transformation, Viralen
dc.subjectComet Assayen
dc.subjectGenome, Viralen
dc.subjectGreen Fluorescent Proteins/genetics/metabolismen
dc.subjectHumansen
dc.subjectHydrogen Peroxide/pharmacologyen
dc.subjectMiceen
dc.subjectNIH 3T3 Cellsen
dc.subjectOxidative Stressen
dc.subjectPlasmidsen
dc.subjectPolymerase Chain Reactionen
dc.subjectRNA-Directed DNA Polymerase/geneticsen
dc.subjectRetroelements/genetics/*physiologyen
dc.subjectSimian virus 40/*physiologyen
dc.subjectTrace Elements/*pharmacologyen
dc.subjectTransfectionen
dc.subject*Up-Regulationen
dc.subjectVanadium/*pharmacologyen
dc.titleVanadium induces VL30 retrotransposition at an unusually high level: a possible carcinogenesis mechanismen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.jmb.2007.09.012-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17920077-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0022283607011862/1-s2.0-S0022283607011862-main.pdf?_tid=b7542fb649b3e3506e67817d19bbc204&acdnat=1333007275_c50b07b2e667b2f6ddd857f2eb0d4111-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2007-
heal.abstractCarcinogenesis by vanadium is thought to occur through induction of DNA-double-strand breaks (DSBs) but its mechanism is not fully understood. We investigated the effect of vanadium on induction of viral-like 30 element (VL30) retrotransposition using a NIH3T3 cell-retrotransposition assay based on a recombinant VL30/EGFP element. Incubation of assay cells with vanadyl sulphate (VOSO(4)) induced retrotransposition frequency in a dose and time-dependent manner, measured by fluorescence-activated cell scanning (FACS) and retrotransposition events were confirmed by UV microscopy and PCR analysis. Among vanadium salts with different valence tested, vanadyl (4+) ions were the most potent retrotransposition inducers. VOSO(4), at 50 muM induced retrotranspositions at an unusually high frequency of up to 0.185 events per cell per generation. VOSO(4), acting at the transcription level, strongly induced VL30 and endogenous reverse transcriptase (enRT) transcripts with maxima at 50 muM and 100 muM of 22 and 18-fold, respectively. VOSO(4)-induced retrotransposition frequency was inhibited by 42% with efavirenz, an inhibitor of enRTs, while paraquat, a DNA-DSBs inducer, had no effect. Furthermore, it was completely abolished with deferoxamine, a metal chelator, while reduced by 75% with N-acetyl-cysteine, a general antioxidant. Remarkably, H(2)O(2) reproduced inducible retrotransposition linking for the first time oxidative stress to induction of retrotransposition. We propose that VOSO(4)-induced VL30 retrotransposition through H(2)O(2) generation may be an alternative mutagenic, DNA-DSBs independent, mechanism leading to carcinogenesis.en
heal.journalNameJ Mol Biolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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