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:

Bailey Damian M1,Taudorf Sarah2,Berg Ronan M G2,Lundby Carsten34,Pedersen Bente K2,Rasmussen Peter3,Møller Kirsten256

Affiliation:

1. Neurovascular Research Laboratory, Faculty of Health, Science and Sport, University of Glamorgan, Glamorgan, UK

2. Department of Infectious Diseases, Centre of Inflammation and Metabolism, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

3. Zurich Centre for Integrative Human Physiology, University of Zurich, Zurich, Switzerland

4. Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

5. Department of Cardiothoracic Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

6. Department of Anaesthesiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark

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.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Clinical Neurology,Neurology

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