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?

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

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)1020 - 1026
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Volume31
Issue number4
DOIs
Publication statusPublished - 9 Feb 2011

Keywords

  • brain
  • free radicals
  • hypoxia
  • mitochondrial oxygen tension
  • oxygen sensing

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