Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure.
Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure.
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暴露于 O2 后灌注大鼠肺中的三羧酸循环活性。
DOI：
10.1152/ajplung.1992.262.4.l495
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Reichenbaugh,SS
中科院分区：
文献类型：
--
作者：
Bassett,DJ;Reichenbaugh,SS
在暴露于空气或100%O2体内18-30 h后，在大鼠分离的完整肺中检查O2诱导的线粒体能量产生损伤。通过分别测量[1- 14 C]丙酮酸和[U-14 C]棕榈酸的14 CO2产生来确定线粒体代谢率，在正常和刺激代谢条件下灌注，所述刺激代谢条件是通过灌注氧化磷酸化解偶联剂2，4-二硝基苯酚（DNP）来实现的。在没有DNP的情况下，O2暴露没有显着改变14 CO2生产从任何基板。DNP增加肺丙酮酸和棕榈酸catenorase到CO2的两倍，在空气暴露的肺，但没有改变14 CO2生产从O2暴露的大鼠分离的肺。这些数据表明，O2诱导的丙酮酸和棕榈酸的最大线粒体代谢的损害，不能解释的组织游离辅酶A的改变或吡啶核苷酸的损失。然而，O2和空气暴露的肺之间的三羧酸循环中间体的稳态水平的比较没有确定异柠檬酸脱氢酶作为O2诱导的酶失活的一个可能的网站。
O2-induced impairment of mitochondrial energy generation was examined in intact lungs isolated from rats after 18-30 h exposure to either air or 100% O2 in vivo. Mitochondrial metabolic rates were determined by separate measurements of 14CO2 production from [1-14C]pyruvate and [U-14C]palmitate, perfused under normal and stimulated metabolic conditions brought about by perfusion with the uncoupler of oxidative phosphorylation, 2,4-dinitrophenol (DNP). In the absence of DNP, O2 exposure did not significantly alter 14CO2 productions from either substrate. DNP increased lung pyruvate and palmitate catabolism to CO2 twofold in air-exposed lungs but did not alter 14CO2 production in lungs isolated from O2-exposed rats. These data demonstrated an O2-induced impairment of maximal mitochondrial metabolism of both pyruvate and palmitate that could not be explained by alterations in tissue free coenzyme A or by loss of pyridine nucleotides. However, comparisons of the steady-state levels of tricarboxylic acid cycle intermediates between O2- and air-exposed lungs did identify isocitrate dehydrogenase as a possible site of O2-induced enzyme inactivation.