Mitochondrial dysfunction and oxidative stress: a contributing link to acquired epilepsy?
Mitochondrial dysfunction and oxidative stress: a contributing link to acquired epilepsy?
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DOI：
10.1007/s10863-010-9320-9
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发表时间：
2010-12
影响因子：
3
通讯作者：
Patel, Manisha
中科院分区：
文献类型：
--
作者：
Waldbaum, Simon;Patel, Manisha
线粒体功能障碍和氧化应激导致几种神经系统疾病，最近被认为与获得性癫痫如颞叶癫痫（TLE）有关。获得性癫痫通常由脑损伤引发，随后是“潜伏期”，由此在脑中发生分子、生物化学和其他细胞改变，导致慢性癫痫。线粒体功能障碍和氧化应激正在成为不仅作为诸如癫痫持续状态（SE）的促发性损伤的结果而急性发生的因素，而且还可能促成癫痫发生和慢性癫痫。线粒体是活性氧（ROS）的主要场所，使其特别容易受到氧化损伤，这可能会影响神经元的兴奋性和癫痫易感性。这个小型审查提供了一个概述的证据表明，线粒体功能障碍和氧化应激的作用，急性损伤的后果，是已知的煽动慢性癫痫及其参与获得性癫痫的慢性阶段。
Mitochondrial dysfunction and oxidative stress contribute to several neurologic disorders and have recently been implicated in acquired epilepsies such as temporal lobe epilepsy (TLE). Acquired epilepsy is typically initiated by a brain injury followed by a “latent period” whereby molecular, biochemical and other cellular alterations occur in the brain leading to chronic epilepsy. Mitochondrial dysfunction and oxidative stress are emerging as factors that not only occur acutely as a result of precipitating injuries such as status epilepticus (SE), but may also contribute to epileptogenesis and chronic epilepsy. Mitochondria are the primary site of reactive oxygen species (ROS) making them uniquely vulnerable to oxidative damage that may affect neuronal excitability and seizure susceptibility. This mini-review provides an overview of evidence suggesting the role of mitochondrial dysfunction and oxidative stress as acute consequences of injuries that are known to incite chronic epilepsy and their involvement in the chronic stages of acquired epilepsy.
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