This study intended to analyze: (1) the effects of acute and severe
hypoxia exposure on skeletal muscle oxidative stress and oxidative damage markers; (2) the protective role of the
antioxidant glutathione against oxidative damage; and (3) the expression of
heat shock protein 70 kDa (HSP70) induced by this hypoxic insult. Forty mice were divided into four groups: control + placebo (C+P),
hypoxia + placebo (H+P), control + l-
buthionine-[ S, R]-sulfoximine (BSO, a GSH-depleting compound) (C+BSO) and
hypoxia + BSO (H+BSO).
Hypoxia groups were continuously exposed for 24 h to a hypobaric hypoxic environment equivalent to an altitude of 7000 m and sacrificed immediately after. Control groups were maintained at sea level during the experimental protocol. Analyzed biochemical parameters were: reduced (GSH) and oxidized (
GSSG)
glutathione,
thiobarbituric acid reactive substances (
TBARS), sulfhydryl
protein groups (SH),
N-acetyl-beta- d-glucosaminidase (NAG) and HSP70
protein.
Hypoxia (H+P) per se, compared to C+P, induced a significant increase in %
GSSG (5.68 vs. 1.14%),
TBARS (436.7 vs. 227.9 nM), NAG (4.49 vs. 3.35 U/mg) and HSP70 (178.7 vs. 100%). Compared with H+P, H+BSO showed a significant decrease in total
glutathione (19.30 vs. 6.13 nmol/mg) and an additional increase in %
GSSG (5.68 vs. 11.33%) and in HSP70 expression (178.7 vs. 202.2%). However, no further oxidative damage was observed in H+BSO. These data suggest that acute
hypoxia per se might enhance oxidative stress; however, the
glutathione system seems to have a modest role in skeletal muscle protection against
hypoxia-induced oxidative stress. Moreover,
hypoxia and BSO treatment is a sufficient stimulus to promote HSP70 overexpression.