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  4. Τμήμα Ιατρικής
  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22920
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dc.contributor.authorGalaris, D.en
dc.contributor.authorEvangelou, A.en
dc.date.accessioned2015-11-24T19:28:42Z-
dc.date.available2015-11-24T19:28:42Z-
dc.identifier.issn1040-8428-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22920-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectCalcium Signaling/drug effectsen
dc.subjectCell Transformation, Neoplastic/*chemically induceden
dc.subjectDNA Damageen
dc.subjectDNA Repair/drug effectsen
dc.subjectFree Radicalsen
dc.subjectHumansen
dc.subjectMAP Kinase Signaling System/drug effectsen
dc.subjectMetals/*adverse effects/pharmacologyen
dc.subjectNeoplasms/chemically induceden
dc.subjectNeoplasms, Experimental/chemically induceden
dc.subject*Oxidative Stressen
dc.subjectTranscription Factors/physiologyen
dc.subjectTranscription, Genetic/drug effectsen
dc.subjectZinc Fingers/drug effectsen
dc.titleThe role of oxidative stress in mechanisms of metal-induced carcinogenesisen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11923071-
heal.identifier.secondaryhttp://www.sciencedirect.com/science/article/pii/S1040842801002128-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractMetals are necessary for the normal functioning of cells and the survival of organisms. However, exposure to higher than the physiological levels of several metals may lead to tumor development. Although the exact molecular mechanism(s) of metal-induced carcinogenesis is not clear, a vast body of evidence indicates that metal-induced generation of reactive oxygen species (ROS) may play a central role in this process. Two main pathways of ROS-induced effects are discussed in this chapter: (i) increased DNA damage induced either directly or indirectly by impeding DNA repair, and (ii) modulation of nuclear transcriptional factor activities, such as NF-kappaB and AP-1, through mitogen-activated protein kinases signal transduction mechanisms.en
heal.journalNameCrit Rev Oncol Hematolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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