{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T13:50:35Z","timestamp":1770817835028,"version":"3.50.1"},"reference-count":62,"publisher":"Portland Press Ltd.","issue":"1","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,1,1]]},"abstract":"<jats:p>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\u00a0h 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\u00a0min exercise bout on a treadmill or remained sedentary 24\u00a0h before receiving either a DOX bolus (20\u00a0mg\/kg of body weight) or saline. Heart and liver mitochondrial function [oxygen consumption, membrane potential (\u0394\u03a8) 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 lag-phase; maximal \u0394\u03a8 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.<\/jats:p>","DOI":"10.1042\/cs20100254","type":"journal-article","created":{"date-parts":[[2010,8,2]],"date-time":"2010-08-02T12:36:07Z","timestamp":1280752567000},"page":"37-49","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":85,"title":["Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats"],"prefix":"10.1042","volume":"120","author":[{"given":"Ant\u00f3nio","family":"Ascens\u00e3o","sequence":"first","affiliation":[{"name":"Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal"}]},{"given":"Jos\u00e9","family":"Lumini-Oliveira","sequence":"additional","affiliation":[{"name":"Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal"},{"name":"Faculty of Health Sciences, University of Fernando Pessoa, Porto, Portugal"}]},{"given":"Nuno\u00a0G.","family":"Machado","sequence":"additional","affiliation":[{"name":"Centre for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal"}]},{"given":"Rita\u00a0M.","family":"Ferreira","sequence":"additional","affiliation":[{"name":"Department of Chemistry, University of Aveiro, Aveiro, Portugal"}]},{"given":"In\u00eas\u00a0O.","family":"Gon\u00e7alves","sequence":"additional","affiliation":[{"name":"Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal"}]},{"given":"Ana\u00a0C.","family":"Moreira","sequence":"additional","affiliation":[{"name":"Centre for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal"}]},{"given":"Franklin","family":"Marques","sequence":"additional","affiliation":[{"name":"Department of Clinical Analysis, Faculty of Pharmacy, University of Porto, Porto, Portugal"},{"name":"Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal"}]},{"given":"Vilma\u00a0A.","family":"Sard\u00e3o","sequence":"additional","affiliation":[{"name":"Centre for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal"}]},{"given":"Paulo\u00a0J.","family":"Oliveira","sequence":"additional","affiliation":[{"name":"Centre for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal"}]},{"given":"Jos\u00e9","family":"Magalh\u00e3es","sequence":"additional","affiliation":[{"name":"Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal"}]}],"member":"288","published-online":{"date-parts":[[2010,9,17]]},"reference":[{"key":"2021113010152576800_B1","doi-asserted-by":"crossref","first-page":"129","DOI":"10.1517\/14740338.7.2.129","article-title":"Drug-induced mitochondrial dysfunction in cardiac and skeletal muscle injury","volume":"7","author":"Sardao","year":"2008","journal-title":"Expert Opin. 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