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dc.contributor.authorHickey, AJR
dc.contributor.authorRenshaw, GMC
dc.contributor.authorSpeers-Roesch, B
dc.contributor.authorRichards, JG
dc.contributor.authorWang, Y
dc.contributor.authorFarrell, AP
dc.contributor.authorBrauner, CJ
dc.date.accessioned2017-11-29T12:00:28Z
dc.date.available2017-11-29T12:00:28Z
dc.date.issued2012
dc.date.modified2013-06-11T03:43:14Z
dc.identifier.issn0174-1578
dc.identifier.doi10.1007/s00360-011-0599-6
dc.identifier.urihttp://hdl.handle.net/10072/47513
dc.description.abstractHypoxia and warm ischemia are primary concerns in ischemic heart disease and transplant and trauma. Hypoxia impacts tissue ATP supply and can induce mitochondrial dysfunction that elevates reactive species release. The epaulette shark, Hemiscyllum ocellatum, is remarkably tolerant of severe hypoxia at temperatures up to 34 C, and therefore provides a valuable model to study warm hypoxia tolerance. Mitochondrial function was tested in saponin permeabilised ventricle fibres using high-resolution respirometry coupled with purpose-built fluorospectrometers. Ventricular mitochondrial function, stability and reactive species production of the epaulette shark was compared with that of the hypoxia-sensitive shovelnose ray, Aptychotrema rostrata. Fibres were prepared from each species acclimated to normoxic water conditions, or following a 2 h, acute hypoxic exposure at levels representing 40% of each species' critical oxygen tension. Although mitochondrial respiratory fluxes for normoxia-acclimated animals were similar for both species, reactive species production in the epaulette shark was approximately half that of the shovelnose ray under normoxic conditions, even when normalised to tissue oxidative phosphorylation flux. The hypoxia-sensitive shovelnose ray halved oxidative phosphorylation flux and cytochrome c oxidase flux was depressed by 34% following hypoxic stress. In contrast, oxidative phosphorylation flux of the epaulette shark ventricular fibres isolated from acute hypoxia exposed the animals remained similar to those from normoxia-acclimated animals. However, uncoupling of respiration revealed depressed electron transport systems in both species following hypoxia exposure. Overall, the epaulette shark ventricular mitochondria showed greater oxidative phosphorylation stability and lower reactive species outputs with hypoxic exposure, and this may protect cardiac bioenergetic function in hypoxic tropical waters.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherSpringer
dc.publisher.placeGermany
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom91
dc.relation.ispartofpageto100
dc.relation.ispartofissue1
dc.relation.ispartofjournalJournal of Comparative Physiology B
dc.relation.ispartofvolume182
dc.rights.retentionY
dc.subject.fieldofresearchMedical Biochemistry and Metabolomics not elsewhere classified
dc.subject.fieldofresearchBiochemistry and Cell Biology
dc.subject.fieldofresearchPhysiology
dc.subject.fieldofresearchZoology
dc.subject.fieldofresearchcode110199
dc.subject.fieldofresearchcode0601
dc.subject.fieldofresearchcode0606
dc.subject.fieldofresearchcode0608
dc.titleA radical approach to beating hypoxia: depressed free radical release from heart fibres of the hypoxia-tolerant epaulette shark (Hemiscyllum ocellatum)
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2012
gro.hasfulltextNo Full Text
gro.griffith.authorRenshaw, Gillian M.


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