| Mitochondrial impairment contributes to cocaine-induced cardiac dysfunction: Prevention by the targeted antioxidant MitoQ. | |
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MedLine Citation:
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PMID: 20566328 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The goal of this study was to assess mitochondrial function and ROS production in an experimental model of cocaine-induced cardiac dysfunction. We hypothesized that cocaine abuse may lead to altered mitochondrial function that in turn may cause left ventricular dysfunction. Seven days of cocaine administration to rats led to an increased oxygen consumption detected in cardiac fibers, specifically through complex I and complex III. ROS levels were increased, specifically in interfibrillar mitochondria. In parallel there was a decrease in ATP synthesis, whereas no difference was observed in subsarcolemmal mitochondria. This uncoupling effect on oxidative phosphorylation was not detectable after short-term exposure to cocaine, suggesting that these mitochondrial abnormalities were a late rather than a primary event in the pathological response to cocaine. MitoQ, a mitochondrial-targeted antioxidant, was shown to completely prevent these mitochondrial abnormalities as well as cardiac dysfunction characterized here by a diastolic dysfunction studied with a conductance catheter to obtain pressure-volume data. Taken together, these results extend previous studies and demonstrate that cocaine-induced cardiac dysfunction may be due to a mitochondrial defect. |
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Authors:
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Aurélia Vergeade; Paul Mulder; Cathy Vendeville-Dehaudt; François Estour; Dominique Fortin; Renée Ventura-Clapier; Christian Thuillez; Christelle Monteil |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-06-04 |
Journal Detail:
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Title: Free radical biology & medicine Volume: 49 ISSN: 1873-4596 ISO Abbreviation: Free Radic. Biol. Med. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-07-27 Completed Date: 2010-12-15 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8709159 Medline TA: Free Radic Biol Med Country: United States |
Other Details:
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Languages: eng Pagination: 748-56 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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INSERM U644, University of Rouen, Rouen F-76183, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / therapeutic use Cocaine Cocaine-Related Disorders / etiology, metabolism, prevention & control Disease Susceptibility Drug Evaluation, Preclinical Heart Diseases / chemically induced, etiology*, metabolism, prevention & control* Male Mitochondria, Heart / drug effects, metabolism, pathology Mitochondrial Diseases / complications*, metabolism Molecular Targeted Therapy Organophosphorus Compounds / pharmacology, therapeutic use* Oxygen Consumption / physiology Rats Rats, Wistar Reactive Oxygen Species / metabolism Ubiquinone / analogs & derivatives*, pharmacology, therapeutic use |
| Chemical | |
Reg. No./Substance:
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0/10-(6'-ubiquinonyl)decyltriphenylphosphonium bromide; 0/Antioxidants; 0/Organophosphorus Compounds; 0/Reactive Oxygen Species; 1339-63-5/Ubiquinone; 50-36-2/Cocaine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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