Magalhães José, Ascensão António, Viscor Ginés, Soares José, Oliveira José, Marques Franklin, Duarte José
Faculty of Sport Sciences, Department of Sport Biology, University of Porto, Porto, Portugal.
Aviat Space Environ Med. 2004 Jan;75(1):16-22.
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.
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).
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.
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.
高原缺氧可能会在人体中诱发氧化应激。然而，急性、严重且未经适应的短期低压缺氧暴露对人体的影响尚未见报道。此外，关于复氧在缺氧时氧化应激程度和损伤标志物方面的混杂作用，人们了解甚少。我们的目标是分析低压缺氧和复氧对血浆氧化应激及氧化损伤的影响。
6名男性志愿者在INEFC - UB低压舱中暴露于模拟海拔5500米（52.52千帕）环境4小时，然后在30分钟内返回海平面。在海平面基线、5500米海拔缺氧1小时和4小时时以及返回海平面后立即收集数据。
观察到急性高山病评分升高（13分）以及动脉血氧饱和度显著变化（在海平面、缺氧4小时和返回海平面时分别为97.5±0.5；53.3±1.9；97.1±0.3%，p<0.05）。从海平面和缺氧1小时与缺氧4小时及返回海平面时相比，总谷胱甘肽（TGSH）含量显著降低（p<0.05）。作为氧化还原氧化变化指标的氧化型谷胱甘肽（%GSSG）百分比显著增加（海平面与1小时；1小时与4小时，以及返回海平面时）。在整个实验过程中，脂质过氧化（TBARS）、蛋白质氧化（SH蛋白质基团）和总抗氧化状态（TAS）遵循谷胱甘肽系统提示的氧化还原变化。
低压缺氧在整个缺氧期间增加了血浆氧化应激和损伤标志物的负担。然而，在复氧期结束时复氧未观察到额外变化。
