Nitric oxide and mitochondria
Nitric oxide and mitochondria
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DOI：
10.2741/2122
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发表时间：
2007-01-01
影响因子：
3.1
通讯作者：
Brown, Guy C.
中科院分区：
文献类型：
--
作者：
Brown, Guy C.
一氧化氮（NO）及其衍生物（活性氮）对线粒体有多种影响，影响细胞生理和细胞死亡。线粒体可以产生和消耗NO， NO刺激线粒体生物发生，显然是通过cGMP上调转录因子。NO通过以下途径抑制线粒体呼吸：(A) NO与O-2竞争时对细胞色素氧化酶的急性可逆抑制，以及(B)活性氮对多个位点的不可逆抑制。NO是一种有效的血管扩张剂（通过cGMP），增加O-2和呼吸底物对线粒体的供应。NO通过呼吸抑制、与泛醇的反应和与膜上O-2的反应刺激线粒体产生活性氧和活性氮。NO主要通过氧化应激诱导细胞凋亡。NO主要通过能量消耗诱导坏死。活性氮激活线粒体通透性过渡孔可引起细胞凋亡或坏死。NO可能通过多种机制保护线粒体介导的细胞死亡。
Nitric oxide ( NO) and its derivatives ( reactive nitrogen species) have multiple effects on mitochondria that impact on cell physiology and cell death. Mitochondria may produce and consume NO and NO stimulates mitochondrial biogenesis, apparently via cGMP upregulation of transcriptional factors. NO inhibits mitochondrial respiration via: ( A) an acute and reversible inhibition of cytochrome oxidase by NO in competition with O-2, and ( B) irreversible inhibition of multiple sites by reactive nitrogen species. NO is a potent vasodilator ( via cGMP), increasing O-2 and respiratory substrate supply to mitochondria. NO stimulates reactive oxygen and nitrogen species production from mitochondria via respiratory inhibition, reaction with ubiquinol and reaction with O-2 in the membrane. NO can induce apoptosis, mainly via oxidative stress. NO induces necrosis, mainly via energy depletion. Reactive nitrogen species activation of the mitochondrial permeability transition pore may cause apoptosis or necrosis. NO may protect against mitochondria-mediated cell death by multiple mechanisms.