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Bailey, D.M. et al.

Damian M. Bailey, Sarah Taudorf, Ronan M. G. Berg, Carsten Lundby, Bente K. Pedersen, Peter Rasmussen, Kirsten Møller,

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?

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.[1]

References

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, D.M., Taudorf, S., Berg, R.M., Lundby, C., Pedersen, B.K., Rasmussen, P., Møller, K. J. Cereb. Blood Flow Metab. (2011) [Pubmed]

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