Difference between revisions of "Scandurra 2010 Adv Exp Med Biol"
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|year=2010 | |year=2010 | ||
|journal=Adv Exp Med Biol | |journal=Adv Exp Med Biol | ||
|abstract=When oxygen supply to tissues is limiting, mitochondrial respiration and ATP production are compromised. To assess the bioenergetic consequences under normoxia and hypoxia, quantitative evaluation of mitochondrial oxygen kinetics is required. Using high-resolution respirometry, the "apparent ''K''<sub>m</sub>" for oxygen or ''p''<sub>50</sub> of respiration in 32D cells was determined at 0.05 +/- 0.01 kPa (0.4 mmHg, 0.5 µM, 0.25% air saturation). Close agreement with ''p''<sub>50</sub> of isolated mitochondria indicates that intracellular gradients are small in small cells at routine activity. At intracellular ''p''<sub>O2</sub> <2 kPa (15 mmHg, 10% air saturation) in various tissues under normoxia, respiration is limited by >2% with a ''p''<sub>50</sub> of 0.05 kPa. Over-estimation of ''p''<sub>50</sub> at 0.4 kPa (3 mmHg) would imply significant (>17%) oxygen limitation of respiration under intracellular normoxia. Based on a critical review, we conclude that ''p''<sub>50</sub> ranges from 0.01 to 0.10 kPa in mitochondria and small cells in the absence of inhibitors of cytochrome ''c'' oxidase, whereas experimental artefacts explain the controversial >200-fold range of ''p''<sub>50</sub> in the literature on mitochondrial oxygen kinetics. | |abstract=When oxygen supply to tissues is limiting, mitochondrial respiration and ATP production are compromised. To assess the bioenergetic consequences under normoxia and hypoxia, quantitative evaluation of mitochondrial oxygen kinetics is required. Using high-resolution respirometry, the "apparent ''K''<sub>m</sub>" for oxygen or ''p''<sub>50</sub> of respiration in 32D cells was determined at 0.05 +/- 0.01 kPa (0.4 mmHg, 0.5 µM, 0.25 % air saturation). Close agreement with ''p''<sub>50</sub> of isolated mitochondria indicates that intracellular gradients are small in small cells at routine activity. At intracellular ''p''<sub>O2</sub> <2 kPa (15 mmHg, 10 % air saturation) in various tissues under normoxia, respiration is limited by >2 % with a ''p''<sub>50</sub> of 0.05 kPa. Over-estimation of ''p''<sub>50</sub> at 0.4 kPa (3 mmHg) would imply significant (>17 %) oxygen limitation of respiration under intracellular normoxia. Based on a critical review, we conclude that ''p''<sub>50</sub> ranges from 0.01 to 0.10 kPa in mitochondria and small cells in the absence of inhibitors of cytochrome ''c'' oxidase, whereas experimental artefacts explain the controversial >200-fold range of ''p''<sub>50</sub> in the literature on mitochondrial oxygen kinetics. | ||
|mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros | |mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
Revision as of 15:56, 24 January 2020
| Scandurra FM, Gnaiger E (2010) Cell respiration under hypoxia: facts and artefacts in mitochondrial oxygen kinetics. Adv Exp Med Biol 662:7-25. |
Scandurra FM, Gnaiger E (2010) Adv Exp Med Biol
Abstract: When oxygen supply to tissues is limiting, mitochondrial respiration and ATP production are compromised. To assess the bioenergetic consequences under normoxia and hypoxia, quantitative evaluation of mitochondrial oxygen kinetics is required. Using high-resolution respirometry, the "apparent Km" for oxygen or p50 of respiration in 32D cells was determined at 0.05 +/- 0.01 kPa (0.4 mmHg, 0.5 µM, 0.25 % air saturation). Close agreement with p50 of isolated mitochondria indicates that intracellular gradients are small in small cells at routine activity. At intracellular pO2 <2 kPa (15 mmHg, 10 % air saturation) in various tissues under normoxia, respiration is limited by >2 % with a p50 of 0.05 kPa. Over-estimation of p50 at 0.4 kPa (3 mmHg) would imply significant (>17 %) oxygen limitation of respiration under intracellular normoxia. Based on a critical review, we conclude that p50 ranges from 0.01 to 0.10 kPa in mitochondria and small cells in the absence of inhibitors of cytochrome c oxidase, whereas experimental artefacts explain the controversial >200-fold range of p50 in the literature on mitochondrial oxygen kinetics.
• O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
Labels: MiParea: Respiration, Instruments;methods
Organism: Mouse
Tissue;cell: Blood cells
Preparation: Intact cells, Isolated mitochondria
Regulation: Oxygen kinetics Coupling state: LEAK, ROUTINE, OXPHOS, ET
HRR: Oxygraph-2k
