Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats
Open accessAbstract
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.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Exercise protects against enhanced mPTP opening in heart mitochondria of rats treated with doxorubicin.
“Similarly, exercise protects against the enhanced mPTP opening in heart mitochondria of rats treated with doxorubicin [288].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [288]
The citation lists haven’t been fetched yet
References 62 · Cited by 103
- Authors
- Ascensão, A., Lumini-Oliveira, J., Machado, N. G., Ferreira, R. M., Gonçalves, I. O., Moreira, A. C., Marques, F., Sardão, V. A., Oliveira, P. J., & Magalhães, J.
- Affiliations
- Universidade do Porto (PT)
- Research Centre in Physical Activity, Health and Leisure, Faculty of Sport Sciences, University of Porto, 4200-450 Porto, Portugal
- Centro de Neurociências e Biologia Celular (PT)
- University of Aveiro (PT)
- Corresponding author
- Ascensão, António
- ORCID
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2010-09-17
- Volume
- 120
- Issue
- 1
- Pages
- 37-49
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W2008714017
- Cited by
- 103
- References
- 62
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 7 · 2023: 7 · 2022: 2 · 2021: 6 · 2020: 8 · 2019: 10 · 2018: 12 · 2017: 7 · 2016: 5 · 2015: 10 · 2014: 5 · 2013: 10 · 2012: 5
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- green
- hal.science
- Licence
- other-oa
- Locations
- Clinical Science (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Chemotherapy-induced cardiotoxicity and mitigation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- acute exercise, doxorubicin, cardiotoxicity, mitochondrial permeability transition pore, cardiac mitochondrial function, endurance exercise, mitochondrial complex I, mitochondrial complex V, superoxide dismutase, caspase-3, caspase-9, apoptosis, cyclophilin D, adenine nucleotide translocase, voltage-dependent anion channel, Bax, Bcl-2, liver mitochondria
- MeSH terms
- Mitochondrial Permeability Transition Pore, Animals, Antibiotics, Antineoplastic, Calcium, Doxorubicin, Male, Mitochondria, Heart, Mitochondria, Liver, Motor Activity, Oxygen Consumption, Superoxide Dismutase, Signal Transduction, Rats, Wistar, Apoptosis, Proton Pumps, Mitochondrial Membrane Transport Proteins, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
