Difference between revisions of "Steinlechner-Maran 1996 Am J Physiol Cell Physiol"
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|journal=Am J Physiol Cell Physiol | |journal=Am J Physiol Cell Physiol | ||
|abstract=We studied the oxygen dependence of respiration in cultured human umbilical vein endothelial cells by use of high-resolution respirometry. The [[ROUTINE respiration |rate of oxygen consumption]] varied from 30 to 50 pmol O<sub>2</sub>ย .s<sup>-1</sup>.10<sup>-6</sup> cells over a sixfold range of cell densities. Respiration was stimulated up to 3.5-fold by uncoupling with [[FCCP |carbonyl cyanide ''p''-trifluoromethoxyphenylhydrazone]] or 2,4-[[dinitrophenol]], and the ''p''<sub>O2</sub> at half-maximal respiration (''p''<sub>50</sub>) increased from 0.05 to 0.12 kPa (0.3 to 0.9 Torr) with respiratory rate. ''p''<sub>50</sub> decreased to a minimum of 0.02 kPa when uncoupled cells were inhibited to control levels. Differences in cell size explained a variation of approximately 0.015 kPa in ''p''<sub>50</sub> at similar respiratory rates per cell. Oxygen diffusion to mitochondria contributed maximally 30% to the regulation of ''p''<sub>50</sub> in coupled cells, as deduced from the shallow slope of the flux dependence of ''p''<sub>50</sub> in uncoupled-inhibited cells compared with the slope in coupled cells. Therefore 70% of the flux dependence of ''p''<sub>50</sub> in coupled cells was caused by changes in metabolic state, which correlated with respiratory rate. | |abstract=We studied the oxygen dependence of respiration in cultured human umbilical vein endothelial cells by use of high-resolution respirometry. The [[ROUTINE respiration |rate of oxygen consumption]] varied from 30 to 50 pmol O<sub>2</sub>ย .s<sup>-1</sup>.10<sup>-6</sup> cells over a sixfold range of cell densities. Respiration was stimulated up to 3.5-fold by uncoupling with [[FCCP |carbonyl cyanide ''p''-trifluoromethoxyphenylhydrazone]] or 2,4-[[dinitrophenol]], and the ''p''<sub>O2</sub> at half-maximal respiration (''p''<sub>50</sub>) increased from 0.05 to 0.12 kPa (0.3 to 0.9 Torr) with respiratory rate. ''p''<sub>50</sub> decreased to a minimum of 0.02 kPa when uncoupled cells were inhibited to control levels. Differences in cell size explained a variation of approximately 0.015 kPa in ''p''<sub>50</sub> at similar respiratory rates per cell. Oxygen diffusion to mitochondria contributed maximally 30% to the regulation of ''p''<sub>50</sub> in coupled cells, as deduced from the shallow slope of the flux dependence of ''p''<sub>50</sub> in uncoupled-inhibited cells compared with the slope in coupled cells. Therefore 70% of the flux dependence of ''p''<sub>50</sub> in coupled cells was caused by changes in metabolic state, which correlated with respiratory rate. | ||
ยป Coupling control protocol: [[CCP 01]] | |||
|mipnetlab=AT Innsbruck Gnaiger E | |mipnetlab=AT Innsbruck Gnaiger E | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology |
Revision as of 12:37, 3 September 2016
Steinlechner-Maran R, Eberl T, Kunc M, Margreiter R, Gnaiger E (1996) Oxygen dependence of respiration in coupled and uncoupled endothelial cells. Am J Physiol Cell Physiol 271:C2053-61. |
Steinlechner-Maran R, Eberl T, Kunc M, Margreiter R, Gnaiger E (1996) Am J Physiol Cell Physiol
Abstract: We studied the oxygen dependence of respiration in cultured human umbilical vein endothelial cells by use of high-resolution respirometry. The rate of oxygen consumption varied from 30 to 50 pmol O2 .s-1.10-6 cells over a sixfold range of cell densities. Respiration was stimulated up to 3.5-fold by uncoupling with carbonyl cyanide p-trifluoromethoxyphenylhydrazone or 2,4-dinitrophenol, and the pO2 at half-maximal respiration (p50) increased from 0.05 to 0.12 kPa (0.3 to 0.9 Torr) with respiratory rate. p50 decreased to a minimum of 0.02 kPa when uncoupled cells were inhibited to control levels. Differences in cell size explained a variation of approximately 0.015 kPa in p50 at similar respiratory rates per cell. Oxygen diffusion to mitochondria contributed maximally 30% to the regulation of p50 in coupled cells, as deduced from the shallow slope of the flux dependence of p50 in uncoupled-inhibited cells compared with the slope in coupled cells. Therefore 70% of the flux dependence of p50 in coupled cells was caused by changes in metabolic state, which correlated with respiratory rate.
ยป Coupling control protocol: CCP 01
โข O2k-Network Lab: AT Innsbruck Gnaiger E
Labels: MiParea: Respiration, mt-Biogenesis;mt-density
Organism: Human
Tissue;cell: Endothelial;epithelial;mesothelial cell
Preparation: Intact cells
Regulation: Oxygen kinetics, Uncoupler Coupling state: ROUTINE, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k