Abstract
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.
Original language | English |
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Pages (from-to) | 1020 - 1026 |
Number of pages | 7 |
Journal | Journal of Cerebral Blood Flow and Metabolism |
Volume | 31 |
Issue number | 4 |
DOIs | |
Publication status | Published - 9 Feb 2011 |
Keywords
- brain
- free radicals
- hypoxia
- mitochondrial oxygen tension
- oxygen sensing