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

    20 Citationer (Scopus)

    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-mitO2) 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-mitO2, but did not affect NSE exchange. These findings suggest that neuro-oxidative stress may constitute an adaptive response.

    OriginalsprogEngelsk
    TidsskriftJournal of Cerebral Blood Flow and Metabolism
    Vol/bind31
    Udgave nummer4
    Sider (fra-til)1020-6
    Antal sider7
    ISSN0271-678X
    DOI
    StatusUdgivet - apr. 2011

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