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?

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

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

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 31, No. 4, 2011, p. 1020-1026.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Bailey, DM, Taudorf, S, Berg, RMG, Lundby, C, Pedersen, BK, Rasmussen, P & Møller, K 2011, '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?', Journal of Cerebral Blood Flow and Metabolism, vol. 31, no. 4, pp. 1020-1026. https://doi.org/10.1038/jcbfm.2011.2

APA

Bailey, D. M., Taudorf, S., Berg, R. M. G., Lundby, C., Pedersen, B. K., Rasmussen, P., & Møller, K. (2011). 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? Journal of Cerebral Blood Flow and Metabolism, 31(4), 1020-1026. https://doi.org/10.1038/jcbfm.2011.2

Vancouver

Bailey DM, Taudorf S, Berg RMG, Lundby C, Pedersen BK, Rasmussen P et al. 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? Journal of Cerebral Blood Flow and Metabolism. 2011;31(4):1020-1026. https://doi.org/10.1038/jcbfm.2011.2

Author

Bailey, Damian M ; Taudorf, Sarah ; Berg, Ronan M G ; Lundby, Carsten ; Pedersen, Bente K ; Rasmussen, Peter ; Møller, Kirsten. / 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?. In: Journal of Cerebral Blood Flow and Metabolism. 2011 ; Vol. 31, No. 4. pp. 1020-1026.

Bibtex

@article{946feb7c0d3e42e58422a0594ec211a0,
title = "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.",
author = "Bailey, {Damian M} and Sarah Taudorf and Berg, {Ronan M G} and Carsten Lundby and Pedersen, {Bente K} and Peter Rasmussen and Kirsten M{\o}ller",
year = "2011",
doi = "10.1038/jcbfm.2011.2",
language = "English",
volume = "31",
pages = "1020--1026",
journal = "Journal of Cerebral Blood Flow and Metabolism",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "4",

}

RIS

TY - JOUR

T1 - 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?

AU - Bailey, Damian M

AU - Taudorf, Sarah

AU - Berg, Ronan M G

AU - Lundby, Carsten

AU - Pedersen, Bente K

AU - Rasmussen, Peter

AU - Møller, Kirsten

PY - 2011

Y1 - 2011

N2 - 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.

AB - 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.

U2 - 10.1038/jcbfm.2011.2

DO - 10.1038/jcbfm.2011.2

M3 - Journal article

VL - 31

SP - 1020

EP - 1026

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

SN - 0271-678X

IS - 4

ER -

ID: 40188239