Oxygen Transport to Tissue XXXI

Volume 662 of the series Advances in Experimental Medicine and Biology pp 7-25


Cell Respiration Under Hypoxia: Facts and Artefacts in Mitochondrial Oxygen Kinetics

  • Francesca M. ScandurraAffiliated withDepartment of General and Transplant Surgery, D. Swarovski Research Laboratory, Medical University of Innsbruck
  • , Erich GnaigerAffiliated withD. Swarovski Research Laboratory, Department of General and Transplant Surgery, Medical University of InnsbruckOROBOROS INSTRUMENTS Email author 


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 m” for oxygen or p 50 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 50 of isolated mitochondria indicates that intracellular gradients are small in small cells at routine activity. At intracellular p O2 <2 kPa (15 mmHg, 10% air saturation) in various tissues under normoxia, respiration is limited by >2% with a p 50 of 0.05 kPa. Over-estimation of p 50 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 50 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 50 in the literature on mitochondrial oxygen kinetics.