Chronic intermittent hypoxia increases rat sternohyoid muscle NADPH oxidase expression with attendant modest oxidative stress

Show simple item record

dc.contributor.author Williams, Robert
dc.contributor.author Lemaire, Paul
dc.contributor.author Lewis, Philip
dc.contributor.author McDonald, Fiona B.
dc.contributor.author Lucking, Eric
dc.contributor.author Hogan, Sean
dc.contributor.author Sheehan, David
dc.contributor.author Healy, Vincent
dc.contributor.author O'Halloran, Ken D.
dc.date.accessioned 2017-01-05T09:36:51Z
dc.date.available 2017-01-05T09:36:51Z
dc.date.issued 2015-01-30
dc.identifier.citation Williams, R., Lemaire, P., Lewis, P., McDonald, F. B., Lucking, E., Hogan, S., Sheehan, D., Healy, V. and O'Halloran, K. D. (2015) 'Chronic intermittent hypoxia increases rat sternohyoid muscle NADPH oxidase expression with attendant modest oxidative stress', Frontiers in Physiology, 6, 15 (9 pp). doi: 10.3389/fphys.2015.00015 en
dc.identifier.volume 6 en
dc.identifier.startpage 15-1 en
dc.identifier.endpage 15-9 en
dc.identifier.issn 1664-042X
dc.identifier.uri http://hdl.handle.net/10468/3428
dc.identifier.doi 10.3389/fphys.2015.00015
dc.description.abstract Chronic intermittent hypoxia (CIH) causes upper airway muscle dysfunction. We hypothesized that the superoxide generating NADPH oxidase (NOX) is upregulated in CIH-exposed muscle causing oxidative stress. Adult male Wistar rats were exposed to intermittent hypoxia (5% O2 at the nadir for 90 s followed by 210 s of normoxia), for 8 h per day for 14 days. The effect of CIH exposure on the expression of NOX subunits, total myosin and 4-hydroxynonenal (4-HNE) protein adducts in sternohyoid muscle was determined by western blotting and densitometry. Sternohyoid protein free thiol and carbonyl group contents were determined by 1D electrophoresis using specific fluorophore probes. Aconitase and glutathione reductase activities were measured as indices of oxidative stress. HIF-1α content and key oxidative and glycolytic enzyme activities were determined. Contractile properties of sternohyoid muscle were determined ex vivo in the absence and presence of apocynin (putative NOX inhibitor). We observed an increase in NOX 2 and p47 phox expression in CIH-exposed sternohyoid muscle with decreased aconitase and glutathione reductase activities. There was no evidence, however, of increased lipid peroxidation or protein oxidation in CIH-exposed muscle. CIH exposure did not affect sternohyoid HIF-1α content or aldolase, lactate dehydrogenase, or glyceraldehyde-3-phosphate dehydrogenase activities. Citrate synthase activity was also unaffected by CIH exposure. Apocynin significantly increased sternohyoid force and power. We conclude that CIH exposure upregulates NOX expression in rat sternohyoid muscle with concomitant modest oxidative stress but it does not result in a HIF-1α-dependent increase in glycolytic enzyme activity. Constitutive NOX activity decreases sternohyoid force and power. Our results implicate NOX-dependent reactive oxygen species in CIH-induced upper airway muscle dysfunction which likely relates to redox modulation of key regulatory proteins in excitation-contraction coupling. en
dc.description.sponsorship University College Cork (Department of Physiology, School of Medicine) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Frontiers Media en
dc.rights © 2015 Williams, Lemaire, Lewis, McDonald, Lucking, Hogan, Sheehan, Healy and O'Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. en
dc.rights.uri https://creativecommons.org/licenses/by/4.0/ en
dc.subject Apocynin en
dc.subject Intermittent hypoxia en
dc.subject NADPH oxidase en
dc.subject Oxidative stress en
dc.subject Respiratory muscle en
dc.subject Sternohyoid, en
dc.subject Sleep apnea en
dc.subject Upper airway en
dc.title Chronic intermittent hypoxia increases rat sternohyoid muscle NADPH oxidase expression with attendant modest oxidative stress en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Ken O'Halloran, Physiology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: k.ohalloran@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2017-01-04T16:55:39Z
dc.description.version Published Version en
dc.internal.rssid 286038144
dc.contributor.funder Health Research Board en
dc.contributor.funder University College Cork en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Frontiers in Physiology en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress k.odonoghue@ucc.ie en


Files in this item

This item appears in the following Collection(s)

Show simple item record

© 2015 Williams, Lemaire, Lewis, McDonald, Lucking, Hogan, Sheehan, Healy and O'Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Except where otherwise noted, this item's license is described as © 2015 Williams, Lemaire, Lewis, McDonald, Lucking, Hogan, Sheehan, Healy and O'Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
This website uses cookies. By using this website, you consent to the use of cookies in accordance with the UCC Privacy and Cookies Statement. For more information about cookies and how you can disable them, visit our Privacy and Cookies statement