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dc.contributor.authorThompson, L.P.
dc.contributor.authorSong, H.
dc.contributor.authorPolster, B.M.
dc.date.accessioned2019-08-05T17:00:30Z
dc.date.available2019-08-05T17:00:30Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85068978199&doi=10.1155%2f2019%2f7210249&partnerID=40&md5=858c88594959aa39d3f05ac0125cc520
dc.identifier.urihttp://hdl.handle.net/10713/10213
dc.description.abstractChronic intrauterine hypoxia is a programming stimulus of cardiovascular dysfunction. While the fetal heart adapts to the reduced oxygenation, the offspring heart becomes vulnerable to subsequent metabolic challenges as an adult. Cardiac mitochondria are key organelles responsible for an efficient energy supply but are subject to damage under hypoxic conditions. We propose that intrauterine hypoxia alters mitochondrial function as an underlying programming mechanism of contractile dysfunction in the offspring. Indices of mitochondrial function such as mitochondrial DNA content, Complex (C) I-V expression, and CI/CIV enzyme activity were measured in hearts of male and female offspring at 90 days old exposed to prenatal hypoxia (10.5% O2) for 14 d prior to term (65 d). Both left ventricular tissue and cardiomyocytes exhibited decreased mitochondrial DNA content, expression of CIV, and CI/CIV activity in male hearts. In female cardiomyocytes, hypoxia had no effect on protein expression of CI-CV nor on CI/CIV activity. This study suggests that chronic intrauterine hypoxia alters the intrinsic properties of select respiratory complexes as a programming mechanism of cardiac dysfunction in the offspring. Sex differences in mitochondrial function may underlie the increased vulnerability of age-matched males compared to females in cardiovascular disease and heart failure.en_US
dc.description.urihttps://doi.org/10.1155/2019/7210249en_US
dc.language.isoen-USen_US
dc.publisherHindawien_US
dc.relation.ispartofOxidative medicine and cellular longevity
dc.subjectchronic intrauterine hypoxiaen_US
dc.subjectcardiovascular dysfunctionen_US
dc.subjectcardiac mitochondriaen_US
dc.titleFetal Programming and Sexual Dimorphism of Mitochondrial Protein Expression and Activity of Hearts of Prenatally Hypoxic Guinea Pig Offspringen_US
dc.typearticleen_US
dc.identifier.doi10.1155/2019/7210249
dc.identifier.pmid31249648


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