Document Detail

Mitochondrial impairment contributes to cocaine-induced cardiac dysfunction: Prevention by the targeted antioxidant MitoQ.
MedLine Citation:
PMID:  20566328     Owner:  NLM     Status:  MEDLINE    
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.
Aurélia Vergeade; Paul Mulder; Cathy Vendeville-Dehaudt; François Estour; Dominique Fortin; Renée Ventura-Clapier; Christian Thuillez; Christelle Monteil
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-04
Journal Detail:
Title:  Free radical biology & medicine     Volume:  49     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-27     Completed Date:  2010-12-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  748-56     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
INSERM U644, University of Rouen, Rouen F-76183, France.
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MeSH Terms
Antioxidants / therapeutic use
Cocaine-Related Disorders / etiology,  metabolism,  prevention & control
Disease Susceptibility
Drug Evaluation, Preclinical
Heart Diseases / chemically induced,  etiology*,  metabolism,  prevention & control*
Mitochondria, Heart / drug effects,  metabolism,  pathology
Mitochondrial Diseases / complications*,  metabolism
Molecular Targeted Therapy
Organophosphorus Compounds / pharmacology,  therapeutic use*
Oxygen Consumption / physiology
Rats, Wistar
Reactive Oxygen Species / metabolism
Ubiquinone / analogs & derivatives*,  pharmacology,  therapeutic use
Reg. No./Substance:
0/10-(6'-ubiquinonyl)decyltriphenylphosphonium bromide; 0/Antioxidants; 0/Organophosphorus Compounds; 0/Reactive Oxygen Species; 1339-63-5/Ubiquinone; 50-36-2/Cocaine

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