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J Cereb Blood Flow Metab. 2011 Apr;31(4):1020-6. doi: 10.1038/jcbfm.2011.2. Epub 2011 Feb 9.

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?

Author information

1
Neurovascular Research Laboratory, Faculty of Health, Science and Sport, University of Glamorgan, Glamorgan, UK. dbailey1@glam.ac.uk

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.

PMID:
21304557
PMCID:
PMC3070986
DOI:
10.1038/jcbfm.2011.2
[Indexed for MEDLINE]
Free PMC Article

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