| Endurance training and chronic intermittent hypoxia modulate in vitro salicylate-induced hepatic mitochondrial dysfunction. | |
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MedLine Citation:
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PMID: 23069012 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Mitochondrial function is modulated by multiple approaches including physical activity, which can afford cross-tolerance against a variety of insults. We therefore aimed to analyze the effects of endurance-training (ET) and chronic-intermittent hypobaric-hypoxia (IHH) on liver mitochondrial bioenergetics and whether these effects translate into benefits against in vitro salicylate mitochondrial toxicity. Twenty-eight young-adult male rats were divided into normoxic-sendentary (NS), normoxic-exercised (NE), hypoxic-sendentary (HS) and hypoxic-exercised (HE). ET consisted of 1h/d of treadmill running and IHH of simulated atmospheric pressure of 49.3kPa 5h/d during 5wks. Liver mitochondrial oxygen consumption, transmembrane-electric potential (ΔΨ) and permeability transition pore induction (MPTP) were evaluated in the presence and absence of salicylate. Aconitase, MnSOD, caspase-3 and 8 activities, -SH, MDA, SIRT3, Cyp D, HSP70, OXPHOS subunit contents were assessed. ET and IHH decreased basal mitochondrial state-3 and state-4 respiration, although no alterations were observed in ΔΨ endpoints evaluated in control mitochondria. In the presence of salicylate, ET and IHH decreased state-4 and lag-phase of ADP-phosphorylarion. Moreover, ADP-lag phase in hypoxic was further lower than in normoxic groups. Neither ET nor IHH altered the susceptibility to calcium-induced MPTP. IHH lowered MnSOD and increased aconitase activities. ET and IHH decreased caspase 8 activity whereas no effect was observed on caspase 3. The levels of SIRT3 increased with ET and IHH and Cyp D decreased with IHH. Data suggest that ET and IHH do not alter general basal liver mitochondrial function, but may attenuate some adverse effects of salicylate. |
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Authors:
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A Ascensão; I O Gonçalves; J Lumini-Oliveira; I Marques-Aleixo; E Dos Passos; S Rocha-Rodrigues; N G Machado; A C Moreira; P J Oliveira; J R Torrella; J Magalhães |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-10-12 |
Journal Detail:
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Title: Mitochondrion Volume: - ISSN: 1872-8278 ISO Abbreviation: Mitochondrion Publication Date: 2012 Oct |
Date Detail:
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Created Date: 2012-10-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100968751 Medline TA: Mitochondrion Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012. Published by Elsevier B.V. |
Affiliation:
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Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, Portugal. Electronic address: aascensao@fade.up.pt. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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