Chandel N, Budinger G R, Kemp R A, Schumacker P T
Department of Medicine, University of Chicago, Illinois 60637, USA.
Am J Physiol. 1995 Jun;268(6 Pt 1):L918-25. doi: 10.1152/ajplung.1995.268.6.L918.
During acute (< 30 min) hypoxia, cellular respiration is independent of the O2 concentration as long as PO2 remains above a critical value (5-10 Torr). Similarly, state 3 respiration by isolated mitochondria is independent of PO2 above a critical tension of 2-4 Torr. However, rat hepatocytes demonstrate a reversible suppression of respiration and an increase in NAD(P)H concentration during prolonged (2-24 h), but not acute hypoxia [P. T. Schumacker, N. Chandel, and A. G. N. Augusti. Am. J. Physiol. 265 (Lung Cell. Mol. Physiol. 9): L395-L402, 1993]. This study tested whether respiration is similarly inhibited in isolated mitochondria exposed to low PO2 for prolonged periods and whether cytochrome-c oxidase participates in this response. Coupled rat liver mitochondria were incubated under low oxygen conditions (PO2 < 2 Torr) for 2 h. State 3 respiration after reoxygenation to PO2 = 20 Torr was then compared with the value obtained subsequently at 100 Torr. Using succinate and ADP as substrates, we determined that state 3 respiration at 20 Torr was 61.0 +/- 8.4% of the subsequent value at 100 Torr (P < 0.05). By contrast, control mitochondria reoxygenated to 100 Torr first and 20 Torr subsequently showed no significant difference at the two O2 tensions (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
在急性（<30分钟）缺氧期间，只要氧分压（PO2）保持在临界值（5 - 10托）以上，细胞呼吸就与氧气浓度无关。同样，分离的线粒体的状态3呼吸在PO2高于2 - 4托的临界张力时与PO2无关。然而，大鼠肝细胞在长时间（2 - 24小时）而非急性缺氧期间表现出呼吸的可逆性抑制和NAD(P)H浓度的增加[P.T.舒马赫、N.钱德尔和A.G.N.奥古斯蒂。《美国生理学杂志》265（肺细胞与分子生理学9）：L395 - L402，1993]。本研究测试了长时间暴露于低PO2的分离线粒体中呼吸是否同样受到抑制，以及细胞色素c氧化酶是否参与了这种反应。将偶联的大鼠肝脏线粒体在低氧条件（PO2 < 2托）下孵育2小时。然后将复氧至PO2 = 20托后的状态3呼吸与随后在100托时获得的值进行比较。使用琥珀酸和ADP作为底物，我们确定20托时的状态3呼吸是随后100托时值的61.0 +/- 8.4%（P < 0.05）。相比之下，先复氧至100托然后再复氧至20托的对照线粒体在两种氧张力下没有显著差异（P = 无显著性差异）。（摘要截断于250字）
