| Melatonin protects against heart ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. | |
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MedLine Citation:
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PMID: 19684190 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Melatonin, a well-known antioxidant, has been shown to protect against ischemia-reperfusion myocardial damage. Mitochondrial permeability transition pore (MPTP) opening is an important event in cardiomyocyte cell death occurring during ischemia-reperfusion and therefore a possible target for cardioprotection. In the present study, we tested the hypothesis that melatonin could protect heart against ischemia-reperfusion injury by inhibiting MPTP opening. Isolated perfused rat hearts were subjected to global ischemia and reperfusion in the presence or absence of melatonin in a Langerdoff apparatus. Melatonin treatment significantly improves the functional recovery of Langerdoff hearts on reperfusion, reduces the infarct size, and decreases necrotic damage as shown by the reduced release of lactate dehydrogenase. Mitochondria isolated from melatonin-treated hearts are less sensitive than mitochondria from reperfused hearts to MPTP opening as demonstrated by their higher resistance to Ca(2+). Similar results were obtained following treatment of ischemic-reperfused rat heart with cyclosporine A, a known inhibitor of MPTP opening. In addition, melatonin prevents mitochondrial NAD(+) release and mitochondrial cytochrome c release and, as previously shown, cardiolipin oxidation associated with ischemia-reperfusion. Together, these results demonstrate that melatonin protects heart from reperfusion injury by inhibiting MPTP opening, probably via prevention of cardiolipin peroxidation. |
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Authors:
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Giuseppe Petrosillo; Giuseppe Colantuono; Nicola Moro; Francesca M Ruggiero; Edy Tiravanti; Nicola Di Venosa; Tommaso Fiore; Giuseppe Paradies |
Publication Detail:
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Type: In Vitro; Journal Article Date: 2009-08-14 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 297 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2009 Oct |
Date Detail:
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Created Date: 2009-09-25 Completed Date: 2009-10-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1487-93 Citation Subset: IM |
Affiliation:
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Department of Biochemistry and Molecular Biology and CNR Institute of Biomembranes and Bioenergetics, Section of Anaesthesia, University of Bari, Bari, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / pharmacology* Calcium / metabolism Cardiolipins / metabolism Cardiovascular Agents / pharmacology* Cyclosporine / pharmacology Cytochromes c / metabolism Heart Rate / drug effects L-Lactate Dehydrogenase / metabolism Lipid Peroxidation / drug effects Male Melatonin / pharmacology* Membrane Potential, Mitochondrial / drug effects Mitochondria, Heart / drug effects*, metabolism Mitochondrial Membrane Transport Proteins / antagonists & inhibitors*, metabolism Myocardial Infarction / metabolism, pathology, physiopathology, prevention & control* Myocardial Reperfusion Injury / metabolism, pathology, physiopathology, prevention & control* Myocardium / metabolism*, pathology NAD / metabolism Necrosis Perfusion Rats Rats, Wistar Recovery of Function Time Factors Ventricular Function, Left / drug effects Ventricular Pressure / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Cardiolipins; 0/Cardiovascular Agents; 0/Mitochondrial Membrane Transport Proteins; 0/mitochondrial permeability transition pore; 53-84-9/NAD; 59865-13-3/Cyclosporine; 73-31-4/Melatonin; 7440-70-2/Calcium; 9007-43-6/Cytochromes c; EC 1.1.1.27/L-Lactate Dehydrogenase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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