Oxidative stress in hepatic ischemia-reperfusion injury: the role of antioxidants and iron chelating compounds (Journal article)

Galaris, D./ Barbouti, A./ Korantzopoulos, P.


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dc.contributor.authorGalaris, D.en
dc.contributor.authorBarbouti, A.en
dc.contributor.authorKorantzopoulos, P.en
dc.date.accessioned2015-11-24T19:00:22Z-
dc.date.available2015-11-24T19:00:22Z-
dc.identifier.issn1381-6128-
dc.identifier.urihttp://olympias.lib.uoi.gr/jspui/handle/123456789/19517-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectAntioxidants/physiology/*therapeutic useen
dc.subjectHumansen
dc.subjectIron Chelating Agents/*therapeutic useen
dc.subjectLiver/*blood supply/drug effects/metabolismen
dc.subjectLiver Diseases/drug therapy/metabolismen
dc.subjectOxidative Stress/drug effects/*physiologyen
dc.subjectReactive Oxygen Species/metabolism/therapeutic useen
dc.subjectReperfusion Injury/drug therapy/*metabolismen
dc.titleOxidative stress in hepatic ischemia-reperfusion injury: the role of antioxidants and iron chelating compoundsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/16918418-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2006-
heal.abstractIschemia-reperfusion (IR) injury is a multifactorial process triggered when the liver or other organs are transiently subjected to reduced blood supply followed by reperfusion. It has been shown that "reactive oxygen species" (ROS) are generated during ischemia and reperfusion and may represent pivotal mediators of the ensuing pathological complications. In some cases, however, moderate production of ROS may exert protective effects, a phenomenon presumably related to "ischemic preconditioning". This review will focus mainly on: a) describing the sources and the biochemical mechanisms of ROS generation during ischemia and reperfusion, b) discussing current developments in understanding the biochemical pathways by which ROS may induce toxic or protective effects, c) critically evaluating the results of previous attempts to counteract the toxic effects of ROS by using a variety of antioxidant and transition metal-chelating agents, and d) if feasible, proposing potential new pharmaceutical agents aimed at ameliorating ROS-inducing deleterious effects during reperfusion. It is concluded that ROS are generated from different sources, at different periods during IR, and may act by a variety of not well understood biochemical mechanisms which ultimately lead to cell damage and tissue failure.en
heal.journalNameCurr Pharm Desen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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