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dc.contributor.authorReichelt, Melissaen_US
dc.contributor.authorShanu, Anaen_US
dc.contributor.authorWillems, Lauraen_US
dc.contributor.authorK. Witting, Paulen_US
dc.contributor.authorA. Ellis, Natashaen_US
dc.contributor.authorR. Blackburn, Michaelen_US
dc.contributor.authorHeadrick, Johnen_US
dc.date.accessioned2017-04-24T08:09:11Z
dc.date.available2017-04-24T08:09:11Z
dc.date.issued2009en_US
dc.date.modified2010-06-16T05:42:15Z
dc.identifier.issn15230864en_US
dc.identifier.doi10.1089/ars.2009.2644en_AU
dc.identifier.urihttp://hdl.handle.net/10072/29430
dc.description.abstractWe tested the impact of A1 adenosine receptor (AR) deletion on injury and oxidant damage in mouse hearts subjected to 25 min ischemia/45 min reperfusion (I/R). Wild-type hearts recovered ~50% of contractile function, and released 8.2ᰮ7 IU/g of lactate dehydrogenase (LDH). A1AR deletion worsened dysfunction and LDH efflux (15.2Ხ6 IU/g). Tissue cholesterol and native cholesteryl esters were unchanged, while cholesteryl ester-derived lipid hydroperoxides and hydroxides (CE-O(O)H; a marker of lipid oxidation) increased 3-fold, and a-tocopherylquinone (a-TQ; oxidation product of a-tocopherol (a-TOH)) increased 6-fold. Elevations in a-TQ were augmented 2- to 3-fold by A1AR deletion, whereas CE-O(O)H was unaltered. A1AR deletion also decreased glutathione redox status ([GSH]/[GSSG+GSH]) and enhanced expression of the antioxidant response element heme oxygenase-1 (HO-1) during I/R: 4-fold elevations in HO-1 mRNA and activity were doubled by A1AR deletion. Broad-spectrum AR agonism (10 占2-chloroadenosine; 2-CAD) countered effects of A1AR deletion on oxidant damage, HO-1, and tissue injury, indicating additional ARs (A2A, A2B and/or A3) can mediate similar actions. These data reveal local adenosine engages A1ARs during I/R to selectively limit oxidant damage and enhance outcome. Control of a-TOH/a-TQ levels may contribute to A1AR-dependent cardioprotection.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherMary Ann Liebert, Inc.en_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom2641en_US
dc.relation.ispartofpageto2650en_US
dc.relation.ispartofissue11en_US
dc.relation.ispartofjournalAntioxidants & Redox Signalingen_US
dc.relation.ispartofvolume11en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchBiochemistry and Cell Biology not elsewhere classifieden_US
dc.subject.fieldofresearchAnimal Physiology - Cellen_US
dc.subject.fieldofresearchCardiology (incl. Cardiovascular Diseases)en_US
dc.subject.fieldofresearchcode060199en_US
dc.subject.fieldofresearchcode060602en_US
dc.subject.fieldofresearchcode110201en_US
dc.titleEndogenous adenosine selectively modulates oxidant stress via the A1 receptor in ischemic heartsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.rights.copyrightCopyright 2009 Mary Ann Liebert, Inc., publishers. Self-archiving of the author-manuscript version is not yet supported by this publisher. Please refer to the journal link for access to the definitive, published version or contact the authors for more information.en_AU
gro.date.issued2009
gro.hasfulltextNo Full Text


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