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-mitO2) 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-mitO2, 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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Journal | Journal of Cerebral Blood Flow and Metabolism |
Volume | 31 |
Issue number | 4 |
Pages (from-to) | 1020-6 |
Number of pages | 7 |
ISSN | 0271-678X |
DOIs | |
Publication status | Published - Apr 2011 |