Harrison 2015 J Appl Physiol: Difference between revisions
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|journal=J Appl Physiol | |journal=J Appl Physiol | ||
|abstract=Mitochondrial control of cellular redox states is a fundamental component of cell signaling in the coordination of core energy metabolism and homeostasis during normoxia and hypoxia. We investigated the relationship between cytochrome redox states and mitochondrial oxygen consumption at steady-state levels of hypoxia in mitochondria isolated from beef and mouse heart (BHImt, MHImt), comparing two species with different cardiac dynamics and local oxygen demands. A low-noise, rapid spectrophotometric system using visible light for the measurement of cytochrome redox states was combined with high-resolution respirometry. Monophasic hyperbolic relations were observed between oxygen consumption, ''J''<sub>O2</sub>, and oxygen partial pressure, ''p''<sub>O2</sub>, within the range <1.1 kPa (8.3 mmHg; 13 ยตM). ''p''<sub>50''j''</sub> (''p''<sub>O2</sub> at 0.5โ''J''<sub>max</sub>) was 0.015ยฑ0.0004 and 0.021ยฑ0.003 kPa (0.11 and 0.16 mmHg) for BHImt and MHImt, respectively. Maximum oxygen consumption, ''J''<sub>max</sub>, was measured at saturating ADP levels (OXPHOS capacity) with Complex I-linked substrate supply. Redox states of cytochromes ''aa''<sub>3</sub> and ''c'' were biphasic hyperbolic functions of ''p''<sub>O2</sub>. The relation between cytochrome oxidation state and oxygen consumption revealed a separation of distinct phases from mild to severe and deep hypoxia. When cytochrome ''c'' oxidation increased from fully reduced to 45% oxidised at 0.1 ''J''<sub>max</sub>, ''p''<sub>O2</sub> was as low as 0.002 kPa (0.02 ยตM), and trace amounts of oxygen are sufficient to partially oxidize the cytochromes. At higher ''p''<sub>O2</sub> under severe hypoxia, respiration increases steeply while redox changes are small. Under mild hypoxia, the steep slope of oxidation of cytochrome ''c'' when flux remains more stable represents a cushioning mechanism maintaining respiration high at the onset of hypoxia. | |abstract=Mitochondrial control of cellular redox states is a fundamental component of cell signaling in the coordination of core energy metabolism and homeostasis during normoxia and hypoxia. We investigated the relationship between cytochrome redox states and mitochondrial oxygen consumption at steady-state levels of hypoxia in mitochondria isolated from beef and mouse heart (BHImt, MHImt), comparing two species with different cardiac dynamics and local oxygen demands. A low-noise, rapid spectrophotometric system using visible light for the measurement of cytochrome redox states was combined with high-resolution respirometry. Monophasic hyperbolic relations were observed between oxygen consumption, ''J''<sub>O2</sub>, and oxygen partial pressure, ''p''<sub>O2</sub>, within the range <1.1 kPa (8.3 mmHg; 13 ยตM). ''p''<sub>50''j''</sub> (''p''<sub>O2</sub> at 0.5โ''J''<sub>max</sub>) was 0.015ยฑ0.0004 and 0.021ยฑ0.003 kPa (0.11 and 0.16 mmHg) for BHImt and MHImt, respectively. Maximum oxygen consumption, ''J''<sub>max</sub>, was measured at saturating ADP levels (OXPHOS capacity) with Complex I-linked substrate supply. Redox states of cytochromes ''aa''<sub>3</sub> and ''c'' were biphasic hyperbolic functions of ''p''<sub>O2</sub>. The relation between cytochrome oxidation state and oxygen consumption revealed a separation of distinct phases from mild to severe and deep hypoxia. When cytochrome ''c'' oxidation increased from fully reduced to 45% oxidised at 0.1 ''J''<sub>max</sub>, ''p''<sub>O2</sub> was as low as 0.002 kPa (0.02 ยตM), and trace amounts of oxygen are sufficient to partially oxidize the cytochromes. At higher ''p''<sub>O2</sub> under severe hypoxia, respiration increases steeply while redox changes are small. Under mild hypoxia, the steep slope of oxidation of cytochrome ''c'' when flux remains more stable represents a cushioning mechanism maintaining respiration high at the onset of hypoxia. | ||
|editor=[[Gnaiger E]] | |||
|mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS | |mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS | ||
}} | }} | ||
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|topics=Oxygen kinetics | |topics=Oxygen kinetics | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
| | |pathways=N | ||
|instruments=Oxygraph-2k, TIP2k, O2k-Spectrophotometer | |instruments=Oxygraph-2k, TIP2k, O2k-Spectrophotometer | ||
|additional=MitoFit news, MitoFitPublication | |additional=MitoFit news, MitoFitPublication | ||
}} | }} | ||
* This publication presents results obtained with a test prototype instrument of the [[NextGen-O2k]]. | ::::* This publication presents results obtained with a test prototype instrument of the [[NextGen-O2k]]. | ||
::::ยป More details: [[NextGen-O2k innovation]] | |||
[[Image:Logo MitoFit.jpg|right|120px|link=http://www.mitofit.org/index.php/MitoFit|MitoFit]] | [[Image:Logo MitoFit.jpg|right|120px|link=http://www.mitofit.org/index.php/MitoFit|MitoFit]] | ||
== MitoFit news 2015#14 == | == MitoFit news 2015#14 == | ||
* 2015-09-02: Defining mt-hypoxia at cytochrome redox steady-states, with the [[NextGen-O2k]]. ยป [[MitoFit news]] | ::::* 2015-09-02: Defining mt-hypoxia at cytochrome redox steady-states, with the [[NextGen-O2k]]. ยป [[MitoFit news]] |
Revision as of 15:54, 7 November 2016
Harrison DK, Fasching M, Fontana-Ayoub M, Gnaiger E (2015) Cytochrome redox states and respiratory control in mouse and beef heart mitochondria at steady-state levels of hypoxia. J Appl Physiol 119:1210-8. |
Harrison DK, Fasching M, Fontana-Ayoub M, Gnaiger E (2015) J Appl Physiol
Abstract: Mitochondrial control of cellular redox states is a fundamental component of cell signaling in the coordination of core energy metabolism and homeostasis during normoxia and hypoxia. We investigated the relationship between cytochrome redox states and mitochondrial oxygen consumption at steady-state levels of hypoxia in mitochondria isolated from beef and mouse heart (BHImt, MHImt), comparing two species with different cardiac dynamics and local oxygen demands. A low-noise, rapid spectrophotometric system using visible light for the measurement of cytochrome redox states was combined with high-resolution respirometry. Monophasic hyperbolic relations were observed between oxygen consumption, JO2, and oxygen partial pressure, pO2, within the range <1.1 kPa (8.3 mmHg; 13 ยตM). p50j (pO2 at 0.5โJmax) was 0.015ยฑ0.0004 and 0.021ยฑ0.003 kPa (0.11 and 0.16 mmHg) for BHImt and MHImt, respectively. Maximum oxygen consumption, Jmax, was measured at saturating ADP levels (OXPHOS capacity) with Complex I-linked substrate supply. Redox states of cytochromes aa3 and c were biphasic hyperbolic functions of pO2. The relation between cytochrome oxidation state and oxygen consumption revealed a separation of distinct phases from mild to severe and deep hypoxia. When cytochrome c oxidation increased from fully reduced to 45% oxidised at 0.1 Jmax, pO2 was as low as 0.002 kPa (0.02 ยตM), and trace amounts of oxygen are sufficient to partially oxidize the cytochromes. At higher pO2 under severe hypoxia, respiration increases steeply while redox changes are small. Under mild hypoxia, the steep slope of oxidation of cytochrome c when flux remains more stable represents a cushioning mechanism maintaining respiration high at the onset of hypoxia.
โข Bioblast editor: Gnaiger E โข O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS
Labels: MiParea: Respiration, Instruments;methods, Comparative MiP;environmental MiP
Organism: Mouse, Bovines
Tissue;cell: Heart
Preparation: Isolated mitochondria
Regulation: Oxygen kinetics Coupling state: OXPHOS Pathway: N HRR: Oxygraph-2k, TIP2k, O2k-Spectrophotometer
MitoFit news, MitoFitPublication
- This publication presents results obtained with a test prototype instrument of the NextGen-O2k.
- ยป More details: NextGen-O2k innovation
MitoFit news 2015#14
- 2015-09-02: Defining mt-hypoxia at cytochrome redox steady-states, with the NextGen-O2k. ยป MitoFit news