Journal of Bioenergetics and Biomembranes

, Volume 27, Issue 6, pp 583–596

Control of mitochondrial and cellular respiration by oxygen

  • Erich Gnaiger
  • Rosmarie Steinlechner-Maran
  • Gabriela Méndez
  • Thomas Eberl
  • Raimund Margreiter
Article

DOI: 10.1007/BF02111656

Cite this article as:
Gnaiger, E., Steinlechner-Maran, R., Méndez, G. et al. J Bioenerg Biomembr (1995) 27: 583. doi:10.1007/BF02111656

Abstract

Control and regulation of mitochondrial and cellular respiration by oxygen is discussed with three aims: (1) A review of intracellular oxygen levels and gradients, particularly in heart, emphasizes the dominance of extracellular oxygen gradients. Intracellular oxygen pressure,\(p_{O_2 } \), is low, typically one to two orders of magnitude below incubation conditions used routinely for the study of respiratory control in isolated mitochondria. The\(p_{O_2 } \) range of respiratory control by oxygen overlaps with cellular oxygen profiles, indicating the significance of\(p_{O_2 } \) in actual metabolic regulation. (2) A methodologically detailed discussion of high-resolution respirometry is necessary for the controversial topic of respiratory control by oxygen, since the risk of methodological artefact is closely connected with far-reaching theoretical implications. Instrumental and analytical errors may mask effects of energetic state and partially explain the divergent views on the regulatory role of intracellular\(p_{O_2 } \). Oxygen pressure for half-maximum respiration,p50, in isolated mitochondria at state 4 was 0.025 kPa (0.2 Torr; 0.3 ΜM O2), whereasp50 in endothelial cells was 0.06–0.08 kPa (0.5 Torr). (3) A model derived from the thermodynamics of irreversible processes was developed which quantitatively accounts for near-hyperbolic flux/\(p_{O_2 } \) relations in isolated mitochondria. The apparentp50 is a function of redox potential and protonmotive force. The protonmotive force collapses after uncoupling and consequently causes a decrease inp50. Whereas it is becoming accepted that flux control is shared by several enzymes, insufficient attention is paid to the notion of complementary kinetic and thermodynamic flux control mechanisms.

Key words

Oxygen limitation p50 critical oxygen pressure respirometry polarographic oxygen sensor human endothelial cells rat liver mitochondria intracellular\(p_{O_2 } \) oxygen gradients kinetics nonequilibrium thermodynamics 

Copyright information

© Plenum Publishing Corporation 1995

Authors and Affiliations

  • Erich Gnaiger
    • 1
  • Rosmarie Steinlechner-Maran
    • 1
  • Gabriela Méndez
    • 2
  • Thomas Eberl
    • 1
  • Raimund Margreiter
    • 1
  1. 1.Department of Transplant SurgeryUniversity Hospital of InnsbruckInnsbruckAustria
  2. 2.Instituto de Investigaciones CardiológicasUniversidad de Buenos AiresBuenos AiresArgentina