Gnaiger 1998 Biochim Biophys Acta

From Bioblast
Revision as of 16:27, 24 April 2023 by Gnaiger Erich (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Publications in the MiPMap
Gnaiger E, Lassnig B, Kuznetsov AV, Margreiter R (1998) Mitochondrial respiration in the low oxygen environment of the cell: Effect of ADP on oxygen kinetics. Biochim Biophys Acta 1365:249-54.

Β» PMID: 9693739 Open Access

Gnaiger Erich, Lassnig B, Kuznetsov AV, Margreiter R (1998) Biochim Biophys Acta

Abstract: Oxygen levels in the intracellular microenvironment of tissues such as heart are extremely low, at 1–2% of standard atmospheric oxygen pressure. Kinetic studies with isolated mitochondria suggest a regulatory role of oxygen under these conditions, particularly in active states at high ADP concentration, when oxygen affinity was lower than in the resting state at ADP limitation. The oxygen pressure at 50% of maximum flux, p50, was 0.035 and 0.057 kPa in heart and liver mitochondria, respiring in State 3 on substrates for Complex I or II and II, respectively. p50 in the resting State 4 was 0.02 kPa. The apparent kinetic efficiency, Jmax/p50, increased from the resting to the active state, despite the decrease of oxygen affinity, 1/p50. Consequently, the relative increase of respiratory flux by ADP activation, expressed as the respiratory acceptor control ratio, declined under hypoxia, but not to the extreme of a complete loss of the scope for activation, which would occur at constant Jmax/p50. High oxygen affinity is achieved by an excess capacity of cytochrome c oxidase relative to the Electron transfer-pathway and a correspondingly low turnover rate of this enzyme, consistent with the concept of kinetic trapping of oxygen [1]. β€’ Keywords: Oxygen affinity, Catalytic efficiency, Respiratory control, Hypoxia, Mitochondrion, Heart, Liver

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


  • State 2 in this publication has the meaning of a LEAK state of respiration, without added adenylates (no ADP and no ATP) in the presence of defined respiratory carbon substrates (different from the definition by Chance, Williams 1955).
  • State 4 in this publication is a LEAK state of respiration induced by addition of defined respiratory carbon substrates and a high concenteration of ATP.
  • State 3 is measured at high [ADP] close to saturated [ADP] (OXPHOS capacity) in the presence of added ATP.
  • State 3u is induced by an optimum concentration of an uncoupler (FCCP) to obtain maximum oxygen flux ET-capacity.


Legend to Fig. 2: Instead of "pO2 was dependent ..." it should read: "p50 was dependent on respiratory rate, but also on metabolic state".

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.

  • 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)

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

Organism: Rat  Tissue;cell: Heart, Liver  Preparation: Isolated mitochondria 

Regulation: ADP, Flux control, Oxygen kinetics, Threshold;excess capacity, Uncoupler  Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, CIV  HRR: Oxygraph-2k 

Tissue normoxia, BEC 2020.2, MitoFit 2021 Tissue normoxia 

Cookies help us deliver our services. By using our services, you agree to our use of cookies.