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?

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% O2). Mitochondrial oxygen tension ([Formula: see text]) 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 [Formula: see text], but did not affect NSE exchange. These findings suggest that neuro-oxidative stress may constitute an adaptive response.