IMPAIRED FUNCTION OF MITOCHONDRIAL ELECTRON-TRANSFER COMPLEX-I IN CANINE MYOCARDIAL ISCHEMIA - LOSS OF FLAVIN MONONUCLEOTIDE
IMPAIRED FUNCTION OF MITOCHONDRIAL ELECTRON-TRANSFER COMPLEX-I IN CANINE MYOCARDIAL ISCHEMIA - LOSS OF FLAVIN MONONUCLEOTIDE
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DOI：
10.1016/0022-2828(83)90329-2
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发表时间：
1983-01-01
影响因子：
5
通讯作者：
RANGANATHAN, S
中科院分区：
文献类型：
--
作者：
ROUSLIN, W;RANGANATHAN, S
在麻醉的狗中，通过阻塞回旋冠状动脉的左分支来产生局部心肌缺血。闭塞30或60分钟后，从左心室和隔膜的非缺血性（对照）和缺血性透壁样品中分离线粒体。来自60分钟缺血心肌的线粒体表现出NAD-连接状态3呼吸速率下降至56 ± 1.5。对照组的3%，并且NADH-CoQ [NADH辅酶Q]还原酶活性平行损失至54 ±-。4%的控制。对分离自60分钟缺血心肌的线粒体中的电子转移复合物I的2种非蛋白质组分的分析显示，酸可提取的FMN减少至58 ± 0.5%。5%的对照，泛醌少量降低至89 ± 0.5%。对照组的2%。观察到的解离和明显的洗脱的非共价结合的FMN从缺血损伤的线粒体，因此占几乎定量的比例减少，看到在NADH-CoQ还原酶活性和状态3呼吸与NAD-连接的底物。
Regional myocardial ischemia was produced in anesthetized dogs by occluding the left branch of the circumflex coronary artery. After 30 or 60 min of occlusion, mitochondria were isolated from both non-ischemic (control) and ischemic transmural samples of the left ventricle and septum. Mitochondria from 60 min ischemic myocardium exhibited a drop in NAD-linked state 3 respiratory rates to 56 .+-. 3% of controls and a parallel loss of NADH-CoQ [NADH coenzyme Q] reductase activity to 54 .+-. 4% of controls. Analysis of 2 non-protein components of electron transfer complex I in mitochondria isolated from 60 min ischemic myocardium revealed a decrease in acid-extractable FMN to 58 .+-. 5% of controls and a small decrease in ubiquinone to 89 .+-. 2% of controls. The observed dissociation and apparent washout of non-covalently-bound FMN from the ischemically damaged mitochondria thus accounted nearly quantitatively for the proportionate decrease seen in NADH-CoQ reductase activity and in state 3 respiration with NAD-linked substrates.