Myocardial ischemia decreases oxidative phosphorylation through cytochrome oxidase in subsarcolemmal mitochondria
Myocardial ischemia decreases oxidative phosphorylation through cytochrome oxidase in subsarcolemmal mitochondria
复制标题
DOI：
10.1152/ajpheart.1997.273.3.h1544
复制
发表时间：
1997-09-01
影响因子：
4.8
通讯作者：
Hoppel, CL
中科院分区：
文献类型：
--
作者：
Lesnefsky, EJ;Tandler, B;Hoppel, CL
采用离体兔心脏，研究了心肌缺血对线粒体氧化磷酸化的影响。经过45分钟的全脑缺血，氧化磷酸化减少，只有在肌膜下人口的线粒体与所有基板测试。N，N，N '，N'四甲基对苯二胺-抗坏血酸盐是一种通过细胞色素c向细胞色素氧化酶提供电子的供体，在肌膜下线粒体中氧化减少[缺血组（n = 6）：76 +/- 3 vs.对照组（n = 5）：105 +/- 6 nanoatoms 0.min（-1）.mg（-1），P < 0.01]，但在原纤维间线粒体中没有。在缺血后的分离的线粒体中，通过电子显微镜观察到只有轻微的形态学变化。无论是细胞色素氧化酶的活性测定条件下的最大活性，也不是明显的米氏常数和最大速度值的两个细胞色素c结合位点是不同的心肌细胞膜下的线粒体分离缺血和对照心脏。缺血后肌膜下线粒体细胞色素c含量降低（缺血组：0.111 ± 0.013vs.对照组：0.156 ± 0.007nmol/mg蛋白，P < 0.05）。因此，缺血降低率氧化磷酸化通过细胞色素氧化酶选择性地在完整的肌膜下线粒体。对电子传递链末端段的缺血性损伤涉及细胞色素c含量的减少，而细胞色素氧化酶的可表达催化活性保持不变。
The effect of myocardial ischemia on mitochondrial oxidative phosphorylation was investigated using isolated, buffer-perfused rabbit hearts. After 45 min of global ischemia, oxidative phosphorylation was decreased only in the subsarcolemmal population of mitochondria with all substrates tested. The oxidation of N,N,N',N' tetramethyl p-phenylenediamine-ascorbate, an electron donor to cytochrome oxidase via cytochrome c, was decreased in subsarcolemmal mitochondria [ischemia (n = 6): 76 +/- 3 vs. control (n = 5): 105 +/- 6 nanoatoms O.min(-1).mg(-1), P < 0.01] but not in interfibrillar mitochondria. Only minor morphological changes were observed by electron microscopy in the isolated mitochondria after ischemia. Neither cytochrome oxidase activity measured under conditions for maximal activity nor the apparent Michaelis constant and maximum velocity values of the two cytochrome c binding sites were different in subsarcolemmal mitochondria isolated from ischemic and control hearts. The cytochrome c content was decreased in subsarcolemmal mitochondria after ischemia (ischemia: 0.111 +/- 0.013 vs. control: 0.156 +/- 0.007 nmol/mg protein, P < 0.05). Thus ischemia decreased the rate of oxidative phosphorylation through cytochrome oxidase selectively in intact subsarcolemmal mitochondria. Ischemic damage to the terminal segment of the electron transport chain involves a decrease in the content of cytochrome c, whereas the expressible catalytic activity of cytochrome oxidase remains unchanged.