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1 Department of Sport Biology, Faculty of Sport Sciences, Porto, Portugal
2 Department of Clinical Analysis and of Biochemistry, Faculty of Pharmacy, Porto, Portugal
* To whom correspondence should be addressed. E-mail: jmaga{at}fcdef.up.pt.
Severe high-altitude hypoxia exposure is considered a triggering stimulus for redox disturbances at distinct levels of cellular organization. The effect of an in-vivo acute and severe hypobaric hypoxic insult (48h at a pressure equivalent to 8500m) on oxidative damage and respiratory function was analyzed in skeletal muscle mitochondria isolated from vitamin E supplemented (60mg.kg-1 i.p., 3 times/wk for 3 wks) and non-supplemented mice. Forty male mice were randomly divided into 4 groups: control+placebo (C+P), hypoxia+placebo (H+P), control+vitamin E (C+V) and hypoxia+vitamin E (H+V). Significant increases in mitochondrial HSP60 expression, protein carbonyls groups (CGs) levels and decrease in aconitase activity and sulfhydryl groups (SH) content were found in the H+P group when compared with the C+P group. Mitochondrial respiration was significantly impaired in animals from the H+P group as demonstrated by decreased state 3, respiratory control ratio (RCR) and ADP/O, and by increased state 4 with both complex I and II-linked substrates. Using malate+pyruvate (MP) as substrates, hypoxia decreased the respiratory rate in the presence of CCCP (carbonyl cyanide m-chlorophenylhydrazone) and also stimulated oligomycin-inhibited respiration. However, vitamin E treatment attenuated the effect of hypoxia on the mitochondrial levels of HSP60 and markers of oxidative stress. Vitamin E was also able to prevent most mitochondrial alterations induced by hypobaric hypoxia. In conclusion, hypobaric hypoxia increases mitochondrial oxidative stress while decreasing mitochondrial capacity for oxidative phosphorylation. Vitamin E was an effective preventive agent which further supports the oxidative character of mitochondrial dysfunction induced by hypoxia.
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