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Article: Phosphatidylcholine metabolism in ischemic and hypoxic hearts

TitlePhosphatidylcholine metabolism in ischemic and hypoxic hearts
Authors
Issue Date1992
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177
Citation
Molecular And Cellular Biochemistry, 1992, v. 116 n. 1-2, p. 53-58 How to Cite?
AbstractThe rates of phosphatidylcholine biosynthesis in the isolated hamster hearts under ischemic and hypoxic conditions were examined. Global ischemia was produced by perfusion of the heart with a reduced flow, whereas hypoxia was produced by perfusion with a N2-saturated buffer. A 51% reduction in the biosynthesis of phosphatidylcholine was observed in the ischemic heart. The reduction was caused by a severe decrease in ATP level which resulted in a diminished conversion of choline into phosphocholine. A 22% reduction in the biosynthetic rate of phosphatidylcholine was also detected in the hypoxic heart. The reduction was caused by a diminished level of CTP which resulted in a decreased conversion of phosphocholine to CDP-choline. No compensatory mechanism was triggered during ischemia, but the CTP : phosphocholine cytidylyltransferase activity was enhanced in the hypoxic heart. Our results demonstrate the possible rate-limiting role of choline kinase and reconfirm the regulatory role of the cytidylyltransferase in the biosynthesis of phosphatidylcholine.
Persistent Identifierhttp://hdl.handle.net/10722/171046
ISSN
2015 Impact Factor: 2.613
2015 SCImago Journal Rankings: 1.019
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChoy, PCen_US
dc.contributor.authorChan, Men_US
dc.contributor.authorHatch, Gen_US
dc.contributor.authorMan, RYKen_US
dc.date.accessioned2012-10-30T06:11:58Z-
dc.date.available2012-10-30T06:11:58Z-
dc.date.issued1992en_US
dc.identifier.citationMolecular And Cellular Biochemistry, 1992, v. 116 n. 1-2, p. 53-58en_US
dc.identifier.issn0300-8177en_US
dc.identifier.urihttp://hdl.handle.net/10722/171046-
dc.description.abstractThe rates of phosphatidylcholine biosynthesis in the isolated hamster hearts under ischemic and hypoxic conditions were examined. Global ischemia was produced by perfusion of the heart with a reduced flow, whereas hypoxia was produced by perfusion with a N2-saturated buffer. A 51% reduction in the biosynthesis of phosphatidylcholine was observed in the ischemic heart. The reduction was caused by a severe decrease in ATP level which resulted in a diminished conversion of choline into phosphocholine. A 22% reduction in the biosynthetic rate of phosphatidylcholine was also detected in the hypoxic heart. The reduction was caused by a diminished level of CTP which resulted in a decreased conversion of phosphocholine to CDP-choline. No compensatory mechanism was triggered during ischemia, but the CTP : phosphocholine cytidylyltransferase activity was enhanced in the hypoxic heart. Our results demonstrate the possible rate-limiting role of choline kinase and reconfirm the regulatory role of the cytidylyltransferase in the biosynthesis of phosphatidylcholine.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177en_US
dc.relation.ispartofMolecular and Cellular Biochemistryen_US
dc.subject.meshAdenosine Triphosphate - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Transporten_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshCholine - Metabolismen_US
dc.subject.meshCholine Kinase - Metabolismen_US
dc.subject.meshCholine-Phosphate Cytidylyltransferaseen_US
dc.subject.meshCricetinaeen_US
dc.subject.meshCytidine Diphosphate Choline - Metabolismen_US
dc.subject.meshCytidine Triphosphate - Metabolismen_US
dc.subject.meshMesocricetusen_US
dc.subject.meshMyocardial Ischemia - Metabolismen_US
dc.subject.meshNucleotidyltransferases - Metabolismen_US
dc.subject.meshPhosphatidylcholines - Metabolismen_US
dc.subject.meshPhosphorylcholine - Metabolismen_US
dc.titlePhosphatidylcholine metabolism in ischemic and hypoxic heartsen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF01270569en_US
dc.identifier.pmid1336121-
dc.identifier.scopuseid_2-s2.0-0026497964en_US
dc.identifier.volume116en_US
dc.identifier.issue1-2en_US
dc.identifier.spage53en_US
dc.identifier.epage58en_US
dc.identifier.isiWOS:A1992JZ20600009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChoy, PC=7006633002en_US
dc.identifier.scopusauthoridChan, M=7402597606en_US
dc.identifier.scopusauthoridHatch, G=7102271713en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US

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