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- Publisher Website: 10.1007/BF01270569
- Scopus: eid_2-s2.0-0026497964
- PMID: 1336121
- WOS: WOS:A1992JZ20600009
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Article: Phosphatidylcholine metabolism in ischemic and hypoxic hearts
Title | Phosphatidylcholine metabolism in ischemic and hypoxic hearts |
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Authors | |
Keywords | biosynthesis hamster heart hypoxia ischemia phosphatidylcholine |
Issue Date | 1992 |
Publisher | Springer 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/171046 |
ISSN | 2023 Impact Factor: 3.5 2023 SCImago Journal Rankings: 0.901 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Choy, PC | en_US |
dc.contributor.author | Chan, M | en_US |
dc.contributor.author | Hatch, G | en_US |
dc.contributor.author | Man, RYK | en_US |
dc.date.accessioned | 2012-10-30T06:11:58Z | - |
dc.date.available | 2012-10-30T06:11:58Z | - |
dc.date.issued | 1992 | en_US |
dc.identifier.citation | Molecular And Cellular Biochemistry, 1992, v. 116 n. 1-2, p. 53-58 | en_US |
dc.identifier.issn | 0300-8177 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171046 | - |
dc.description.abstract | The 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.language | eng | en_US |
dc.publisher | Springer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177 | en_US |
dc.relation.ispartof | Molecular and Cellular Biochemistry | en_US |
dc.subject | biosynthesis | - |
dc.subject | hamster heart | - |
dc.subject | hypoxia | - |
dc.subject | ischemia | - |
dc.subject | phosphatidylcholine | - |
dc.subject.mesh | Adenosine Triphosphate - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Biological Transport | en_US |
dc.subject.mesh | Cell Hypoxia | en_US |
dc.subject.mesh | Choline - Metabolism | en_US |
dc.subject.mesh | Choline Kinase - Metabolism | en_US |
dc.subject.mesh | Choline-Phosphate Cytidylyltransferase | en_US |
dc.subject.mesh | Cricetinae | en_US |
dc.subject.mesh | Cytidine Diphosphate Choline - Metabolism | en_US |
dc.subject.mesh | Cytidine Triphosphate - Metabolism | en_US |
dc.subject.mesh | Mesocricetus | en_US |
dc.subject.mesh | Myocardial Ischemia - Metabolism | en_US |
dc.subject.mesh | Nucleotidyltransferases - Metabolism | en_US |
dc.subject.mesh | Phosphatidylcholines - Metabolism | en_US |
dc.subject.mesh | Phosphorylcholine - Metabolism | en_US |
dc.title | Phosphatidylcholine metabolism in ischemic and hypoxic hearts | en_US |
dc.type | Article | en_US |
dc.identifier.email | Man, RYK:rykman@hkucc.hku.hk | en_US |
dc.identifier.authority | Man, RYK=rp00236 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1007/BF01270569 | en_US |
dc.identifier.pmid | 1336121 | - |
dc.identifier.scopus | eid_2-s2.0-0026497964 | en_US |
dc.identifier.volume | 116 | en_US |
dc.identifier.issue | 1-2 | en_US |
dc.identifier.spage | 53 | en_US |
dc.identifier.epage | 58 | en_US |
dc.identifier.isi | WOS:A1992JZ20600009 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Choy, PC=7006633002 | en_US |
dc.identifier.scopusauthorid | Chan, M=7402597606 | en_US |
dc.identifier.scopusauthorid | Hatch, G=7102271713 | en_US |
dc.identifier.scopusauthorid | Man, RYK=7004986435 | en_US |
dc.identifier.issnl | 0300-8177 | - |