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dc.contributor.authorBundgaard, Amanda
dc.contributor.authorJames, Andrew M
dc.contributor.authorJoyce, William
dc.contributor.authorMurphy, Michael P
dc.contributor.authorFago, Angela
dc.date.accessioned2018-07-04T09:04:19Z
dc.date.available2018-07-04T09:04:19Z
dc.date.issued2018-04-25
dc.identifier.issn0022-0949
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/277788
dc.description.abstractFreshwater turtles (Trachemys scripta) are among the very few vertebrates capable of tolerating severe hypoxia and re-oxygenation without suffering from damage to the heart. As myocardial ischemia and reperfusion causes a burst of mitochondrial reactive oxygen species (ROS) in mammals, the question arises as to whether, and if so how, this ROS burst is prevented in the turtle heart. We find that heart mitochondria isolated from turtles acclimated to anoxia produce less ROS than mitochondria from normoxic turtles when consuming succinate. As succinate accumulates in the hypoxic heart and is oxidized when oxygen returns, this suggests an adaptation to lessen ROS production. Specific S-nitrosation of complex I can lower ROS in mammals and here we show that turtle complex I activity and ROS production can also be strongly depressed in vitro by S-nitrosation. We detect in vivo endogenous S-nitrosated complex I in turtle heart mitochondria, but these levels are unaffected upon anoxia acclimation. Thus, while heart mitochondria from anoxia-acclimated turtles generate less ROS and have a lower aerobic capacity than those from normoxic turtles, this is not due to decreases in complex I activity or expression levels. Interestingly, in-gel activity staining reveals that most complex I of heart mitochondria from normoxic and anoxic turtles forms stable super-complexes with other respiratory enzymes and, in contrast to mammals, these are not disrupted by dodecyl maltoside. Taken together, these results show that although S-nitrosation of complex I is a potent mechanism to prevent ROS formation upon re-oxygenation after anoxia in vitro, this is not a major cause of the suppression of ROS production by anoxic turtle heart mitochondria.
dc.format.mediumElectronic
dc.languageeng
dc.publisherThe Company of Biologists
dc.subjectMitochondria, Heart
dc.subjectAnimals
dc.subjectTurtles
dc.subjectOxygen
dc.subjectReactive Oxygen Species
dc.subjectSuccinic Acid
dc.subjectElectron Transport Complex I
dc.subjectGlucosides
dc.subjectAdaptation, Physiological
dc.subjectNitrosation
dc.subjectHypoxia
dc.titleSuppression of reactive oxygen species generation in heart mitochondria from anoxic turtles: the role of complex I S-nitrosation.
dc.typeArticle
prism.issueIdentifierPt 8
prism.publicationDate2018
prism.publicationNameJ Exp Biol
prism.volume221
dc.identifier.doi10.17863/CAM.25126
dcterms.dateAccepted2018-02-26
rioxxterms.versionofrecord10.1242/jeb.174391
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-04-25
dc.contributor.orcidFago, Angela [0000-0001-7315-2628]
dc.identifier.eissn1477-9145
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (G1002277)
pubs.funder-project-idMedical Research Council (MC_U105663142)
pubs.funder-project-idBiotechnology and Biological Sciences Research Council (BB/I012923/1)
pubs.funder-project-idMedical Research Council (MC_EX_MR/M015769/1)
pubs.funder-project-idMedical Research Council (MC_UU_00015/3)
pubs.funder-project-idWellcome Trust (110159/Z/15/Z)
cam.issuedOnline2018-04-25
rioxxterms.freetoread.startdate2019-04-25


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