Document Detail


Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats.
MedLine Citation:
PMID:  20666733     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The use of DOX (doxorubicin), an antibiotic used in oncological treatments, is limited by a dose-related cardiotoxicity against which acute exercise is protective. However, the mitochondrial-related mechanisms of this protection remain unknown. Therefore the present study aimed to determine the effects of an acute endurance exercise bout performed 24 h before DOX treatment on heart and liver mitochondrial function. A total of 20 adult male Wistar rats were divided into groups as follows: non-exercised with saline (NE + SAL), non-exercised DOX-treated (NE + DOX), exercised with saline (EX + SAL) and exercised DOX-treated (EX + DOX). The animals performed a 60 min exercise bout on a treadmill or remained sedentary 24 h before receiving either a DOX bolus (20 mg/kg of body weight) or saline. Heart and liver mitochondrial function [oxygen consumption, membrane potential (DeltaPsi) and cyclosporin-A-sensitive calcium-induced MPTP (mitochondrial permeability transition pore) opening] were evaluated. The activities of the respiratory complex, Mn-SOD (superoxide dismutase), caspases 3 and 9, as well as the levels of ANT (adenine nucleotide translocase), VDAC (voltage-dependent anion channel), CypD (cyclophilin D), Bax and Bcl-2, were measured. Acute exercise prevented the decreased cardiac mitochondrial function (state 3, phosphorylative lagphase; maximal DeltaPsi generated both with complex I- and II-linked substrates and calcium-induced MPTP opening) induced by DOX treatment. Exercise also prevented the DOX-induced decreased activity of cardiac mitochondrial chain complexes I and V, and increased caspase 3 and 9 activities. DOX administration and exercise caused increased cardiac mitochondrial SOD activity. Exercise ameliorated liver mitochondrial complex activities. No alterations were observed in the measured MPTP and apoptosis-related proteins in heart and liver mitochondria. The results demonstrate that acute exercise protects against cardiac mitochondrial dysfunction, preserving mitochondrial phosphorylation capacity and attenuating DOX-induced decreased tolerance to MPTP opening.
Authors:
António Ascensão; José Lumini-Oliveira; Nuno G Machado; Rita M Ferreira; Inês O Gonçalves; Ana C Moreira; Franklin Marques; Vilma A Sardão; Paulo J Oliveira; José Magalhães
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  120     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-09-22     Completed Date:  2010-11-23     Revised Date:  2011-05-05    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  37-49     Citation Subset:  IM    
Affiliation:
Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal. aascensao@fcdef.up.pt
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibiotics, Antineoplastic / pharmacology*
Apoptosis / drug effects,  physiology
Calcium / metabolism,  physiology
Doxorubicin / pharmacology*
Male
Mitochondria, Heart / drug effects*,  metabolism,  physiology
Mitochondria, Liver / drug effects,  metabolism,  physiology
Mitochondrial Membrane Transport Proteins / metabolism*
Motor Activity / physiology*
Oxygen Consumption / drug effects,  physiology
Proton Pumps / metabolism
Rats
Rats, Wistar
Signal Transduction / drug effects,  physiology
Superoxide Dismutase / metabolism
Chemical
Reg. No./Substance:
0/Antibiotics, Antineoplastic; 0/Mitochondrial Membrane Transport Proteins; 0/Proton Pumps; 0/mitochondrial permeability transition pore; 23214-92-8/Doxorubicin; 7440-70-2/Calcium; EC 1.15.1.1/Superoxide Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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