Lipid peroxidation in brain or spinal cord mitochondria after injury.
Lipid peroxidation in brain or spinal cord mitochondria after injury.
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DOI：
10.1007/s10863-015-9600-5
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发表时间：
2016-04
影响因子：
3
通讯作者：
Singh IN
中科院分区：
文献类型：
--
作者：
Hall ED;Wang JA;Bosken JM;Singh IN
大量证据表明，氧自由基形成（即氧化应激）作为脑或脊髓原发性机械损伤后发生的继发性损伤过程的介导物具有重要作用。氧自由基诱导的氧化损伤的主要形式是发生在受损的神经组织脂质过氧化（LP）。受损神经细胞中的大部分氧化应激最初通过产生活性氮物质过亚硝酸盐（PN）而在线粒体中开始，然后产生多种高活性自由基，包括二氧化氮（·NO2）、羟基自由基（·OH）和碳酸根自由基（·CO3）。每一种都可以容易地在线粒体的磷脂膜内诱导LP，导致呼吸功能障碍、钙缓冲障碍、线粒体渗透性转变和细胞死亡。LP在中枢神经系统继发性损伤中的作用已被多种抗氧化剂的线粒体和神经保护作用所证实，并对其进行了简要综述。
Extensive evidence has demonstrated an important role of oxygen radical formation (i.e. oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO2), hydroxyl radical (•OH) and carbonate radical (•CO3). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed.