Oxidative stress in humans during and after 4 hours of hypoxia at a simulated altitude of 5500 m.

Background: High-altitude hypoxia may induce oxidative stress in humans. However, the effect of acute, severe, and non-acclimatized short-term hypobaric hypoxia exposure in humans has not been described. Additionally, little is known regarding the confounding role of reoxygenation in the extent of oxidative stress and damage markers in hypoxia. Our goals were to analyze the effect of of hypobaric hypoxia and reoxygenation on plasma oxidative stress and oxidative damage.

Methods: There were six male volunteers exposed to a simulated altitude of 5500 m (52.52 kPa) in the INEFC-UB hypobaric chamber over 4 h and returned to sea level (SL) in 30 min. Data were collected at baseline SL at 1 h and 4 h of hypoxia at 5500 m and immediately after return to sea level (RSL).

Results: Elevated scores of acute mountain sickness (13) and significant changes in arterial oxygen saturation (97.5 +/- 0.5; 53.3 +/- 1.9; 97.1 +/- 0.3%, p < 0.05 at SL, 4 h, and RSL, respectively) were observed. Significant reductions (p < 0.05) on total glutathione (TGSH) content were measured from SL and 1 h vs. 4 h and RSL. The percentage of oxidized glutathione (%GSSG) as an indicator of redox oxidative changes increased significantly (SL vs. 1 h; 1 h vs. 4 h, and RSL). Lipid peroxidation (TBARS), protein oxidation (SH protein groups), and total antioxidant status (TAS) followed the redox changes suggested by the glutathione system throughout the protocol.

Conclusions: Hypobaric hypoxia increased the burden of plasma oxidative stress and damage markers all through the hypoxia period. However, no additional changes were observed with reoxygenation at the end of the reoxygenation period.