Neurovascular Research Laboratory, Faculty of Health, Science and Sport, University of Glamorgan, Glamorgan, UK.
J Cereb Blood Flow Metab. 2011 Apr;31(4):1020-6. doi: 10.1038/jcbfm.2011.2. Epub 2011 Feb 9.
Cellular hypoxia triggers a homeostatic increase in mitochondrial free radical signaling. In this study, blood was obtained from the radial artery and jugular venous bulb in 10 men during normoxia and 9 hours hypoxia (12.9% O(2)). Mitochondrial oxygen tension (p(O(2))(mit)) was derived from cerebral blood flow and blood gases. The ascorbate radical (A(•-)) was detected by electron paramagnetic resonance spectroscopy and neuron-specific enolase (NSE), a biomarker of neuronal injury, by enzyme-linked immunosorbent assay. Hypoxia increased the cerebral output of A(•-) in proportion to the reduction in p(O(2))(mit), but did not affect NSE exchange. These findings suggest that neuro-oxidative stress may constitute an adaptive response.
细胞缺氧会引发线粒体自由基信号的代偿性增加。在这项研究中，10 名男性在常氧和 9 小时缺氧（12.9% O2）期间分别从桡动脉和颈内静脉球取血。线粒体氧分压（p（O2）（mit））由脑血流和血气得出。电子顺磁共振波谱法检测抗坏血酸自由基（A（•-）），酶联免疫吸附试验检测神经元特异性烯醇化酶（NSE），后者是神经元损伤的生物标志物。缺氧使 A（•-）的脑输出与 p（O2）（mit）的降低成比例增加，但不影响 NSE 交换。这些发现表明，神经氧化应激可能构成一种适应性反应。
