scholarly journals Quantification of Cytochrome C Oxidase and tissue oxygenation using CW-NIRS in mouse cerebral cortex

2021 ◽  
Author(s):  
Mada Hashem ◽  
Ying Wu ◽  
Jeff Dunn
Keyword(s):  
Cerebral Cortex ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Tissue Oxygenation ◽  
Mouse Cerebral Cortex

scholarly journals Hyperoxia results in increased aerobic metabolism following acute brain injury

2016 ◽  
Vol 37 (8) ◽  
pp. 2910-2920 ◽  
Author(s):  
Arnab Ghosh ◽  
David Highton ◽  
Christina Kolyva ◽  
Ilias Tachtsidis ◽  
Clare E Elwell ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Tissue Oxygenation ◽  
Cerebral Blood Flow Velocity ◽  
Oxygenation Index ◽  
Aerobic Metabolism ◽  
Acute Brain Injury ◽  
Cerebral Microdialysis ◽  
Terminal Electron Acceptor

Acute brain injury is associated with depressed aerobic metabolism. Below a critical mitochondrial pO2 cytochrome c oxidase, the terminal electron acceptor in the mitochondrial respiratory chain, fails to sustain oxidative phosphorylation. After acute brain injury, this ischaemic threshold might be shifted into apparently normal levels of tissue oxygenation. We investigated the oxygen dependency of aerobic metabolism in 16 acutely brain-injured patients using a 120-min normobaric hyperoxia challenge in the acute phase (24–72 h) post-injury and multimodal neuromonitoring, including transcranial Doppler ultrasound-measured cerebral blood flow velocity, cerebral microdialysis-derived lactate-pyruvate ratio (LPR), brain tissue pO2 (pbrO2), and tissue oxygenation index and cytochrome c oxidase oxidation state (oxCCO) measured using broadband spectroscopy. Increased inspired oxygen resulted in increased pbrO2 [ΔpbrO2 30.9 mmHg p < 0.001], reduced LPR [ΔLPR −3.07 p = 0.015], and increased cytochrome c oxidase (CCO) oxidation (Δ[oxCCO] + 0.32 µM p < 0.001) which persisted on return-to-baseline (Δ[oxCCO] + 0.22 µM, p < 0.01), accompanied by a 7.5% increase in estimated cerebral metabolic rate for oxygen ( p = 0.038). Our results are consistent with an improvement in cellular redox state, suggesting oxygen-limited metabolism above recognised ischaemic pbrO2 thresholds. Diffusion limitation or mitochondrial inhibition might explain these findings. Further investigation is warranted to establish optimal oxygenation to sustain aerobic metabolism after acute brain injury.

Nitric Oxide Synthase and Cytochrome C Oxidase Changes in the Tumoural and Peritumoural Cerebral Cortex

2001 ◽  
Vol 143 (9) ◽  
pp. 897-908 ◽  
Author(s):  
D. Garbossa ◽  
M. Fontanella ◽  
C. A. Pagni ◽  
A. Vercelli
Keyword(s):  
Nitric Oxide ◽  
Cerebral Cortex ◽  
Nitric Oxide Synthase ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Oxide Synthase

Changes of mitochondrial cytochrome c oxidase and FoF1 ATP synthase subunits in rat cerebral cortex during aging

1995 ◽  
Vol 20 (12) ◽  
pp. 1465-1470 ◽  
Author(s):  
V. G. Nicoletti ◽  
E. A. Tendi ◽  
C. Lalicata ◽  
S. Reale ◽  
A. Costa ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Atp Synthase ◽  
Rat Cerebral Cortex ◽  
Mitochondrial Cytochrome ◽  
Fof1 Atp Synthase ◽  
Mitochondrial Cytochrome C
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