Institute of Neurosciences, Lithuanian University of Health Sciences, Kaunas, Lithuania.
FEBS J. 2013 Oct;280(20):4999-5014. doi: 10.1111/febs.12353. Epub 2013 Jun 18.
We review research investigating mitochondrial damage during heart and brain ischaemia, focusing on the mechanisms and consequences of ischaemia-induced and/or reperfusion-induced: (a) inhibition of mitochondrial respiratory complex I; (b) release of cytochrome c from mitochondria; (c) changes to mitochondrial phospholipids; and (d) nitric oxide inhibition of mitochondria. Heart ischaemia causes inhibition of cytochrome oxidase and complex I, release of cytochrome c, and induction of permeability transition and hydrolysis and oxidation of mitochondrial phospholipids, but some of the mechanisms are unclear. Brain ischaemia causes inhibition of complexes I and IV, but other effects are less clear.
我们综述了研究心脏和大脑缺血期间线粒体损伤的文献，重点关注缺血诱导和/或再灌注诱导的以下机制和后果：（a）线粒体呼吸复合物 I 抑制；（b）细胞色素 c 从线粒体释放；（c）线粒体磷脂变化；以及（d）一氧化氮抑制线粒体。心脏缺血导致细胞色素氧化酶和复合物 I 抑制、细胞色素 c 释放、通透性转换诱导以及线粒体磷脂水解和氧化，但一些机制尚不清楚。脑缺血导致复合物 I 和 IV 抑制，但其他影响不太清楚。
