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dc.contributor.authorVenardos, Kylieen_US
dc.contributor.authorHarrison, Glennen_US
dc.contributor.authorHeadrick, Johnen_US
dc.contributor.authorPerkins, Anthonyen_US
dc.description.abstract1. Auranofin, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and glutathione peroxidase. These enzymes play an important role in protecting cardiac tissue from oxidative stress generated during ischaemia-reperfusion. 2. Auranofin (100 mg/kg) was administered to rats and their hearts were subjected to an in vitro model of ischaemia-reperfusion. The activity of thioredoxin reductase and glutathione peroxidase was determined in liver and heart tissues in an attempt to correlate enzymatic activity with heart recovery after ischaemia-reperfusion. 3. There was significantly less thioredoxin reductase activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of auranofin used was able to selectively inhibit one of these enzyme systems. Rats administered auranofin displayed significantly impaired recovery from ischaemic insult. The end diastolic pressure was increased, whereas the rate pressure product was significantly decreased. 4. The level of postischaemic apoptosis was also assessed by examining caspase-3 activity in tissue homogenates. Auranofin significantly increased the degree of postischaemic apoptosis, leading to poor postischaemic recovery.en_US
dc.publisherBlackwell Publishing Asiaen_US
dc.relation.ispartofjournalClinical and Experimental Pharmacology and Physiologyen_US
dc.subject.fieldofresearchHISTORY AND ARCHAEOLOGYen_US
dc.titleAuranofin increases apoptosis and ischaemia-reperfusion injury in the rat isolated hearten_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 2004 Blackwell Publishing. The definitive version is available at []en_AU
gro.hasfulltextNo Full Text

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