Mitochondrial superoxide production and respiratory activity: biphasic response to ischemic duration.

Mitochondrial superoxide production and respiratory activity: biphasic response to ischemic duration.
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线粒体超氧化物的产生和呼吸活动:对缺血持续时间的双相反应。

DOI:
10.1016/j.abb.2009.01.006
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发表时间:
2009
影响因子:
3.9
通讯作者:
Humphries,KennethM
Humphries,KennethM
中科院分区:
生物学3区
文献类型:
--
作者:
Matsuzaki,Satoshi;Szweda,LukeI;Humphries,KennethM

文献摘要

被引文献

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长时间的缺血与电子传递链缺陷和自由基产生增加有关。相比之下,关于短暂缺血对线粒体功能和自由基产生的影响知之甚少。这项研究的目的是检查缺血持续时间、对电子传递链活性的影响以及线粒体自由基产生之间的关系。使大鼠心脏经历增加的缺血持续时间,分离线粒体,并测量超氧化物产生和电子传递链活性。结果表明,即使短暂的缺血持续时间也会引起超氧化物产生的显着增加。当缺血持续时间少于 15 分钟时,该速率得以维持,然后随着缺血时间的延长而进一步增加。从机制上讲,短暂缺血伴随着 NADH 氧化酶活性的增加,这反映在复合物 IV 活性的特定增加上。相反,较长的缺血持续时间伴随着 NADH 氧化酶活性的降低,这反映在复合物 I 和 IV 活性的缺陷上。
Long bouts of ischemia are associated with electron transport chain deficits and increases in free radical production. In contrast, little is known regarding the effect of brief ischemia on mitochondrial function and free radical production. This study was undertaken to examine the relationship between the duration of ischemia, effects upon electron transport chain activities, and the mitochondrial production of free radicals. Rat hearts were subjected to increasing ischemic durations, mitochondria were isolated, and superoxide production and electron transport chain activities were measured. Results indicate that even brief ischemic durations induced a significant increase in superoxide production. This rate was maintained with ischemic durations less than 15min, and then increased further with longer ischemic times. Mechanistically, brief ischemia was accompanied by an increase in NADH oxidase activity, reflected by a specific increase in complex IV activity. In contrast, longer ischemic durations were accompanied by a decrease in NADH oxidase activity, reflected by deficits in complexes I and IV activities.