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Endurance training and chronic intermittent hypoxia modulate in vitro salicylate-induced hepatic mitochondrial dysfunction.
MedLine Citation:
PMID:  23069012     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  JOURNAL ARTICLE     Date:  2012-10-12
Journal Detail:
Title:  Mitochondrion     Volume:  -     ISSN:  1872-8278     ISO Abbreviation:  Mitochondrion     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100968751     Medline TA:  Mitochondrion     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier B.V.
Affiliation:
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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