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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.

journal of cerebral blood flow and metabolism

Cerebral Formation of Free Radicals during Hypoxia Does Not Cause Structural Damage and is Associated with a Reduction in Mitochondrial PO<sub>2</sub>; Evidence of O<sub>2</sub>-Sensing in Humans?

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?

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?