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dc.contributor.authorReichelt, Melissa E
dc.contributor.authorShanu, Anu
dc.contributor.authorWillems, Laura
dc.contributor.authorWitting, Paul K
dc.contributor.authorEllis, Natasha A
dc.contributor.authorBlackburn, Michael R
dc.contributor.authorHeadrick, John P
dc.date.accessioned2017-05-03T11:16:46Z
dc.date.available2017-05-03T11:16:46Z
dc.date.issued2009
dc.date.modified2010-06-16T05:42:15Z
dc.identifier.issn1523-0864
dc.identifier.doi10.1089/ars.2009.2644
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.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherMary Ann Liebert, Inc.
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom2641
dc.relation.ispartofpageto2650
dc.relation.ispartofissue11
dc.relation.ispartofjournalAntioxidants & Redox Signaling
dc.relation.ispartofvolume11
dc.rights.retentionY
dc.subject.fieldofresearchBiochemistry and cell biology
dc.subject.fieldofresearchBiochemistry and cell biology not elsewhere classified
dc.subject.fieldofresearchAnimal physiology - cell
dc.subject.fieldofresearchMedical biochemistry and metabolomics
dc.subject.fieldofresearchCardiology (incl. cardiovascular diseases)
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences
dc.subject.fieldofresearchcode3101
dc.subject.fieldofresearchcode310199
dc.subject.fieldofresearchcode310909
dc.subject.fieldofresearchcode3205
dc.subject.fieldofresearchcode320101
dc.subject.fieldofresearchcode3214
dc.titleEndogenous adenosine selectively modulates oxidant stress via the A1 receptor in ischemic hearts
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.facultyGriffith Health, School of Medical Science
gro.rights.copyright© 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.
gro.date.issued2009
gro.hasfulltextNo Full Text
gro.griffith.authorHeadrick, John P.


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