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Article: Antioxidant N-acetylcysteine restores myocardial Mn-SOD activity and attenuates myocardial dysfunction in diabetic rats

TitleAntioxidant N-acetylcysteine restores myocardial Mn-SOD activity and attenuates myocardial dysfunction in diabetic rats
Authors
Issue Date2006
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2006, v. 544 n. 1-3, p. 118-125 How to Cite?
AbstractManganese-containing superoxide dismutase (Mn-SOD) plays a critical role in guarding against mitochondrial oxidative stress. Abnormal myocardial mitochondrial metabolism of reactive oxygen species plays an important role in the pathogenesis of diabetic cardiac dysfunction. We hypothesised that chronic treatment with N-acetylcysteine, an antioxidant and glutathione (GSH) precursor, would normalize hyperglycemia induced inactivation of Mn-SOD and attenuate myocardial dysfunction. Control and streptozotozin-induced diabetic rats were treated or untreated with N-acetylcysteine in drinking water for 8 weeks, initiated 1 week after streptozotozin injection. Myocardial performance was determined using the isolated perfused working heart preparation. Myocardial Mn-SOD activity, but not Mn-SOD protein expression, in diabetic rats was significantly reduced while levels of oxidative stress as determined by myocardial free 15-F2t-isoprostane were increased in diabetic rats and were normalized by N-acetylcysteine treatment. However, compensatory increases in myocardial Cu/Zn-SOD and GSH content were seen in diabetic rats accompanied by an increase in tissue antioxidant capacity as compared to control. N-acetylcysteine abolished the compensatory increase in myocardial Cu/Zn-SOD. The left ventricular developed pressure and rates of left ventricular pressure development and relaxation were decreased in diabetic rats as compared to control. These effects were attenuated, but not prevented by N-acetylcysteine treatment. N-acetylcysteine attenuation of diabetic myocardial dysfunction could be attributed to the restoration of myocardial Mn-SOD activity. © 2006 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147233
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorGuo, Zen_US
dc.contributor.authorNagareddy, PRen_US
dc.contributor.authorYuen, Ven_US
dc.contributor.authorYeung, Een_US
dc.contributor.authorMcneill, JHen_US
dc.date.accessioned2012-05-29T06:00:56Z-
dc.date.available2012-05-29T06:00:56Z-
dc.date.issued2006en_US
dc.identifier.citationEuropean Journal Of Pharmacology, 2006, v. 544 n. 1-3, p. 118-125en_US
dc.identifier.issn0014-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/147233-
dc.description.abstractManganese-containing superoxide dismutase (Mn-SOD) plays a critical role in guarding against mitochondrial oxidative stress. Abnormal myocardial mitochondrial metabolism of reactive oxygen species plays an important role in the pathogenesis of diabetic cardiac dysfunction. We hypothesised that chronic treatment with N-acetylcysteine, an antioxidant and glutathione (GSH) precursor, would normalize hyperglycemia induced inactivation of Mn-SOD and attenuate myocardial dysfunction. Control and streptozotozin-induced diabetic rats were treated or untreated with N-acetylcysteine in drinking water for 8 weeks, initiated 1 week after streptozotozin injection. Myocardial performance was determined using the isolated perfused working heart preparation. Myocardial Mn-SOD activity, but not Mn-SOD protein expression, in diabetic rats was significantly reduced while levels of oxidative stress as determined by myocardial free 15-F2t-isoprostane were increased in diabetic rats and were normalized by N-acetylcysteine treatment. However, compensatory increases in myocardial Cu/Zn-SOD and GSH content were seen in diabetic rats accompanied by an increase in tissue antioxidant capacity as compared to control. N-acetylcysteine abolished the compensatory increase in myocardial Cu/Zn-SOD. The left ventricular developed pressure and rates of left ventricular pressure development and relaxation were decreased in diabetic rats as compared to control. These effects were attenuated, but not prevented by N-acetylcysteine treatment. N-acetylcysteine attenuation of diabetic myocardial dysfunction could be attributed to the restoration of myocardial Mn-SOD activity. © 2006 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_US
dc.relation.ispartofEuropean Journal of Pharmacologyen_US
dc.subject.meshAcetylcysteine - Metabolism - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Pharmacologyen_US
dc.subject.meshDiabetes Mellitus, Experimental - Drug Therapy - Pathologyen_US
dc.subject.meshFree Radical Scavengers - Pharmacologyen_US
dc.subject.meshHeart Diseases - Drug Therapy - Pathologyen_US
dc.subject.meshImmunoenzyme Techniquesen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Enzymologyen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.titleAntioxidant N-acetylcysteine restores myocardial Mn-SOD activity and attenuates myocardial dysfunction in diabetic ratsen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ejphar.2006.06.033en_US
dc.identifier.pmid16859669-
dc.identifier.scopuseid_2-s2.0-33746647309en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746647309&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume544en_US
dc.identifier.issue1-3en_US
dc.identifier.spage118en_US
dc.identifier.epage125en_US
dc.identifier.isiWOS:000239856700016-
dc.publisher.placeNetherlandsen_US

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