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Difference between revisions of "Gnaiger 2001 Respir Physiol"

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{{Publication
{{Publication
|title=Gnaiger E (2001) Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply. Respir Physiol 128: 277-297.
|title=Gnaiger E (2001) Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply. Respir Physiol 128:277-97.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/11718759 PMID: 11718759]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/11718759 PMID: 11718759], [[File:PDF.jpg|100px|link=http://www.bioblast.at/images/9/9e/Gnaiger_2001_Respir_Physiol.pdf |Bioblast pdf]]
|authors=Gnaiger E
|authors=Gnaiger Erich
|year=2001
|year=2001
|journal=Respir Physiol
|journal=Respir Physiol
|abstract=Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome c oxidase. Both perspectives relate to the critical oxygen pressure which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/P<sub>50</sub>) are reviewed with particular emphasis on the turnover effect under control of ADP, which increases the P<sub>2</sub> in active states. ADP/O<sub>2</sub> flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ADP/O<sub>2</sub> flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing.
|abstract=Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome ''c'' oxidase. Both perspectives relate to the critical oxygen pressure which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/''p''<sub>50</sub>) are reviewed with particular emphasis on the turnover effect under control of ADP, which increases the ''p''<sub>2</sub> in active states. ~P/O<sub>2</sub> flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ~P/O<sub>2</sub> flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing.
|keywords=Energy: Oxidative phosphorylation, Adenosine diphosphate kinetics, Adenosine diphosphate/O<sub>2</sub> ratio; Hypoxia: Mitochondrial O<sub>2</sub> kinetics, Mammals: Rat, Membrane permeability, Mitochondria: Heart, Liver
|keywords=Energy: Oxidative phosphorylation, Adenosine diphosphate kinetics, Adenosine diphosphate/O<sub>2</sub> ratio; Hypoxia: Mitochondrial O<sub>2</sub> kinetics, Mammals: Rat, Membrane permeability, Mitochondria: Heart, Liver
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck MitoCom
|mipnetlab=AT Innsbruck Gnaiger E
|articletype=Protocol; Manual
|discipline=Mitochondrial Physiology
}}
}}
{{Labeling
{{Labeling
|area=Respiration, Instruments and methods
|area=Respiration, Instruments;methods, Comparative MiP;environmental MiP
|injuries=Oxidative stress;RONS
|organism=Human, Rat
|organism=Human, Rat
|tissues=Heart, Liver, Endothelial; Epithelial; Mesothelial Cell
|tissues=Heart, Liver, Endothelial;epithelial;mesothelial cell, HUVEC
|model cell lines=HUVEC
|preparations=Isolated mitochondria, Intact cells
|preparations=Intact cells, Isolated Mitochondria
|topics=ADP, Coupling efficiency;uncoupling, Oxygen kinetics, Threshold;excess capacity
|injuries=Hypoxia, RONS; Oxidative Stress
|topics=Oxygen kinetics
|couplingstates=OXPHOS
|couplingstates=OXPHOS
|kinetics=ADP; Pi
|instruments=Oxygraph-2k, TIP2k
|instruments=Oxygraph-2k, TIP2k
|additional=Instrumental and methodological aspects
|additional=Tissue normoxia, ATP, Steady state, BEC 2020.1, BEC 2020.2, MitoFit 2021 MgG, MitoFit 2021 Dark respiration, MitoFit 2021 CoQ, MitoFit 2021 Photosynthesis, MitoFit 2021 Yeast, MitoFit 2021 AmR, MitoFit 2021 Tissue normoxia
|articletype=Protocol; Manual
|discipline=Mitochondrial Physiology
}}
}}
[[File:Gnaiger 2001 Respir Physiol New Fig10.jpg|255px|left|thumb|link=]]
[[File:Gnaiger 2001 Respir Physiol New Fig10.jpg|255px|left|thumb|link=]]
'''Fig. 10''' (modified): Opposite effects of ADP limitation and oxygen limitation on mitochondrial membrane potential, and [[LEAK respiration|LEAK oxygen flux]], ''J''<sub>''L'',O2</sub>. The LEAK state is obtained when total oxygen flux equals LEAK respiration. In all other [[respiratory state]]s, total oxygen flux is the sum of LEAK oxygen flux and mechanistically coupled oxygen flux. '''A''': ADP limitation of respiration at high oxygen levels in the transition from the [[OXPHOS]] state (''P'', saturating ADP) or active [[State 3]] (high ADP) to the resting LEAK state, ''L'' (compare [[State 4]]), leads to an increase of membrane potential and exponential acceleration of the proton leak (heavy line). Because LEAK oxygen flux increases while total oxygen flux is reduced, the [[ATP yield]] (ADP/O<sub>2</sub> flux ratio) declines to zero. Turnover-dependent proton leak increases the LEAK oxygen flux in the OXPHOS state but declines towards the LEAK state ([[Garlid_1993_BTK|Garlid et al 1993]]). Mitochondrial production of reactive oxygen species (ROS) increases with membrane potential towards the LEAK state, and ROS-linked electron bypass (electron leak) contributes minimally to LEAK oxygen flux at high oxygen ([[Gnaiger 2000 Proc Natl Acad Sci USA|Gnaiger et al 2000]]). On the right, the decline of ADP/O<sub>2</sub> flux ratios is shown in the transition from OXPHOS to LEAK.Β  '''B''': Oxygen limitation of respiration causes a reduction of membrane potential in the transition from ADP limitation at high oxygen, to intracellular conditions of low oxygen and low ADP, to finally severe oxygen limitation under hypoxia and anoxia. Potentially synergistic with the well documented membrane potential effect on LEAK flux, are the hypothetical effects of decreasing membrane permeability and suppression of ROS production under severe hypoxia, whereas intermediary levels of hypoxia may increase ROS production (modified from Gnaiger 2001; see original publication for further references).
'''Fig. 10''' (modified): Opposite effects of ADP limitation and oxygen limitation on mitochondrial membrane potential, and [[LEAK respiration|LEAK oxygen flux]], ''J''<sub>O2,''L''</sub>. The LEAK state is obtained when total oxygen flux equals LEAK respiration. In all other [[respiratory state]]s, total oxygen flux is the sum of LEAK oxygen flux and mechanistically coupled oxygen flux. '''A''': ADP limitation of respiration at high oxygen levels in the transition from the [[OXPHOS]] state (''P'', saturating ADP) or active [[State 3]] (high ADP) to the resting LEAK state, ''L'' (compare [[State 4]]), leads to an increase of membrane potential and exponential acceleration of the proton leak (heavy line). Because LEAK oxygen flux increases while total oxygen flux is reduced, the [[ATP yield]] (ADP/O<sub>2</sub> flux ratio) declines to zero. Turnover-dependent proton leak increases the LEAK oxygen flux in the OXPHOS state but declines towards the LEAK state ([[Garlid_1993_BTK|Garlid et al 1993]]). Mitochondrial production of reactive oxygen species (ROS) increases with membrane potential towards the LEAK state, and ROS-linked electron bypass (electron leak) contributes minimally to LEAK oxygen flux at high oxygen ([[Gnaiger 2000 Proc Natl Acad Sci U S A|Gnaiger et al 2000]]). On the right, the decline of ~P/O<sub>2</sub> flux ratios is shown in the transition from OXPHOS to LEAK.Β  '''B''': Oxygen limitation of respiration causes a reduction of membrane potential in the transition from ADP limitation at high oxygen, to intracellular conditions of low oxygen and low ADP, to finally severe oxygen limitation under hypoxia and anoxia. Potentially synergistic with the well documented membrane potential effect on LEAK flux, are the hypothetical effects of decreasing membrane permeability and suppression of ROS production under severe hypoxia, whereas intermediary levels of hypoxia may increase ROS production (modified from Gnaiger 2001; see original publication for further references).


Β  * For further discussion, see [[Permeabilized_muscle_fibres#Oxygen_dependence_of_ROS_production_-_are_permeabilized_fibres_a_valid_model.3F|'''Oxygen dependence of ROS production - are permeabilized fibres a valid model?''']].
Β  * Discussion: [[Permeabilized_muscle_fibers#Oxygen_dependence_of_ROS_production_-_are_permeabilized_fibers_a_valid_model.3F|'''Oxygen dependence of ROS production - are permeabilized fibers a valid model?''']].
Β 
Β 
== Cited by ==
{{Template:Cited by Gnaiger 2020 BEC MitoPathways}}
{{Template:Cited by Gnaiger 2020 BEC MitoPhysiology}}
{{Template:Cited by Cardoso 2021 MitoFit MgG}}
{{Template:Cited by Huete-Ortega M 2021 MitoFit Dark respiration}}
{{Template:Cited by Komlodi 2021 MitoFit CoQ}}
{{Template:Cited by Huete-Ortega M 2021 MitoFit Photosynthesis protocols}}
{{Template:Cited by Sobotka 2021 MitoFit Yeast}}
{{Template:Cited by Komlodi 2021 MitoFit AmR}}
{{Template:Cited by Komlodi 2021 MitoFit Tissue normoxia}}

Revision as of 07:08, 16 July 2021

Publications in the MiPMap
Gnaiger E (2001) Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply. Respir Physiol 128:277-97.

Β» PMID: 11718759, Bioblast pdf

Gnaiger Erich (2001) Respir Physiol

Abstract: Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome c oxidase. Both perspectives relate to the critical oxygen pressure which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/p50) are reviewed with particular emphasis on the turnover effect under control of ADP, which increases the p2 in active states. ~P/O2 flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ~P/O2 flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing. β€’ Keywords: Energy: Oxidative phosphorylation, Adenosine diphosphate kinetics, Adenosine diphosphate/O2 ratio; Hypoxia: Mitochondrial O2 kinetics, Mammals: Rat, Membrane permeability, Mitochondria: Heart, Liver

β€’ O2k-Network Lab: AT Innsbruck Gnaiger E


Labels: MiParea: Respiration, Instruments;methods, Comparative MiP;environmental MiP 

Stress:Oxidative stress;RONS  Organism: Human, Rat  Tissue;cell: Heart, Liver, Endothelial;epithelial;mesothelial cell, HUVEC  Preparation: Isolated mitochondria, Intact cells 

Regulation: ADP, Coupling efficiency;uncoupling, Oxygen kinetics, Threshold;excess capacity  Coupling state: OXPHOS 

HRR: Oxygraph-2k, TIP2k 

Tissue normoxia, ATP, Steady state, BEC 2020.1, BEC 2020.2, MitoFit 2021 MgG, MitoFit 2021 Dark respiration, MitoFit 2021 CoQ, MitoFit 2021 Photosynthesis, MitoFit 2021 Yeast, MitoFit 2021 AmR, MitoFit 2021 Tissue normoxia 

Gnaiger 2001 Respir Physiol New Fig10.jpg

Fig. 10 (modified): Opposite effects of ADP limitation and oxygen limitation on mitochondrial membrane potential, and LEAK oxygen flux, JO2,L. The LEAK state is obtained when total oxygen flux equals LEAK respiration. In all other respiratory states, total oxygen flux is the sum of LEAK oxygen flux and mechanistically coupled oxygen flux. A: ADP limitation of respiration at high oxygen levels in the transition from the OXPHOS state (P, saturating ADP) or active State 3 (high ADP) to the resting LEAK state, L (compare State 4), leads to an increase of membrane potential and exponential acceleration of the proton leak (heavy line). Because LEAK oxygen flux increases while total oxygen flux is reduced, the ATP yield (ADP/O2 flux ratio) declines to zero. Turnover-dependent proton leak increases the LEAK oxygen flux in the OXPHOS state but declines towards the LEAK state (Garlid et al 1993). Mitochondrial production of reactive oxygen species (ROS) increases with membrane potential towards the LEAK state, and ROS-linked electron bypass (electron leak) contributes minimally to LEAK oxygen flux at high oxygen (Gnaiger et al 2000). On the right, the decline of ~P/O2 flux ratios is shown in the transition from OXPHOS to LEAK. B: Oxygen limitation of respiration causes a reduction of membrane potential in the transition from ADP limitation at high oxygen, to intracellular conditions of low oxygen and low ADP, to finally severe oxygen limitation under hypoxia and anoxia. Potentially synergistic with the well documented membrane potential effect on LEAK flux, are the hypothetical effects of decreasing membrane permeability and suppression of ROS production under severe hypoxia, whereas intermediary levels of hypoxia may increase ROS production (modified from Gnaiger 2001; see original publication for further references).

* Discussion: Oxygen dependence of ROS production - are permeabilized fibers a valid model?.


Cited by

Gnaiger 2020 BEC MitoPathways
Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002


Gnaiger Erich et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1.
Gnaiger E et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1. doi:10.26124/bec:2020-0001.v1.


  • Cardoso et al (2021) Magnesium Green for fluorometric measurement of ATP production does not interfere with mitochondrial respiration. Bioenerg Commun 2021.1. doi:10.26124/bec:2021-0001
  • Huete-Ortega et al (2021) Substrate-uncoupler-inhibitor-titration protocols for dark respiration in Chlamydomonas reinhardtii. MitoFit Preprints 2021 (in prep).
  • KomlΓ³di T, Cardoso LHD, Doerrier C, Moore AL, Rich PR, Gnaiger E (2021) Coupling and pathway control of coenzyme Q redox state and respiration in isolated mitochondria. Bioenerg Commun 2021.3. https://doi.org/10.26124/bec:2021-0003
  • Huete-Ortega et al (2021) Substrate-uncoupler-inhibitor-titration protocols for photosynthesis in Chlamydomonas reinhardtii. MitoFit Preprints 2021 (in prep).

Template:Cited by Sobotka 2021 MitoFit Yeast

  • KomlΓ³di T, Schmitt S, Zdrazilova L, Donnelly C, Zischka H, Gnaiger E. Oxygen dependence of hydrogen peroxide production in isolated mitochondria and permeabilized cells. MitoFit Preprints (in prep).
  • Komlodi et al (2022) Hydrogen peroxide production, mitochondrial membrane potential and the coenzyme Q redox state measured at tissue normoxia and experimental hyperoxia in heart mitochondria. MitoFit Preprints 2021 (in prep)