Department of General and Transplant Surgery, D. Swarovski Research Laboratory, Medical University of Innsbruck, Innsbruck, Austria.
Adv Exp Med Biol. 2010;662:7-25. doi: 10.1007/978-1-4419-1241-1_2.
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 microM, 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.
当组织的氧气供应受到限制时，线粒体呼吸和 ATP 产生就会受到影响。为了评估常氧和缺氧下的生物能量学后果，需要对线粒体氧动力学进行定量评估。使用高分辨率呼吸计，在 32D 细胞中测定了 0.05 +/- 0.01 kPa（0.4 mmHg、0.5 microM、0.25%空气饱和度）下的氧或呼吸的“表观 K（m）”（p50）。与分离线粒体的 p50 非常吻合，表明在常规活动中小细胞的细胞内梯度很小。在常氧下各种组织中的细胞内 p（O2）<2 kPa（15 mmHg、10%空气饱和度）时，呼吸受到限制，p50 为 0.05 kPa，限制超过 2%。在 0.4 kPa（3 mmHg）时高估 p50，将意味着在细胞内常氧下呼吸受到显著（>17%）的氧气限制。基于一项批判性回顾，我们得出结论，在不存在细胞色素 c 氧化酶抑制剂的情况下，线粒体和小细胞中的 p50 范围为 0.01 至 0.10 kPa，而文献中关于线粒体氧动力学的有争议的 p50 范围超过 200 倍，这是由于实验性人为因素造成的。
