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|104||Cerebral formation of free radicals during hypoxia does not cause structural damage and is associated with a reduction in mitochondrial PO2; evidence of O2-sensing in humans?|
Bailey DM; Taudorf S; Berg RM; Lundby C; Pedersen BK; Rasmussen P; Moller K
J Cereb Blood Flow Metab 2011; 31(4): 1020-6
PubMed ID: 21304557
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.