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% 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.

• Authors: Damian M Bailey, Sarah Taudorf, Ronan M G Berg, Carsten Lundby, Bente K Pedersen, Peter Rasmussen, Kirsten Møller
• Journal: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism (J Cereb Blood Flow Metab) Vol. 31 Issue 4 Pg. 1020-6 (Apr 2011) ISSN: 1559-7016 [Electronic] United States
• PMID: 21304557 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Free Radicals
• Phosphopyruvate Hydratase
• Ascorbic Acid
• Oxygen

Topics

• Adult
• Ascorbic Acid (metabolism)
• Blood Gas Analysis
• Brain Chemistry
• Cerebrovascular Circulation (physiology)
• Free Radicals (metabolism)
• Headache (etiology)
• Homeostasis (physiology)
• Humans
• Hypoxia, Brain (metabolism, pathology)
• Kinetics
• Male
• Mitochondria (metabolism)
• Oxidative Stress
• Oxygen (metabolism)
• Oxygen Consumption (physiology)
• Phosphopyruvate Hydratase (metabolism)