Chan P H
Department of Neurosurgery, Stanford University School of Medicine, California 94205-5487, USA.
J Cereb Blood Flow Metab. 2001 Jan;21(1):2-14. doi: 10.1097/00004647-200101000-00002.
Reactive oxygen species have been implicated in brain injury after ischemic stroke. These oxidants can react and damage the cellular macromolecules by virtue of the reactivity that leads to cell injury and necrosis. Oxidants are also mediators in signaling involving mitochondria, DNA repair enzymes, and transcription factors that may lead to apoptosis after cerebral ischemia. Transgenic or knockout mice with cell- or site-specific prooxidant and antioxidant enzymes provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury.
活性氧已被认为与缺血性中风后的脑损伤有关。这些氧化剂可凭借其反应活性与细胞大分子发生反应并造成损伤,进而导致细胞损伤和坏死。氧化剂还是涉及线粒体、DNA修复酶及转录因子的信号传导介质,可能导致脑缺血后的细胞凋亡。具有细胞或位点特异性促氧化剂和抗氧化酶的转基因或基因敲除小鼠,为剖析缺血性脑损伤信号传导及损伤过程中涉及氧化应激的事件提供了有用的工具。