Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
J Bioenerg Biomembr. 2010 Dec;42(6):461-5. doi: 10.1007/s10863-010-9321-8.
Epilepsy is considered one of the most common neurological disorders worldwide. The burst firing neurons associated with prolonged epileptic discharges could lead to a large number of changes with events of cascades at the cellular level. From its role as the cellular powerhouse, mitochondria also play a crucial role in the mechanisms of cell death. Emerging evidence has shown that prolonged seizures may result in mitochondrial dysfunction and increase of oxidative and nitrosative stress in the hippocampus that precede neuronal cell death and cause subsequent epileptogenesis. The selective dysfunction of mitochondrial respiratory chain Complex I has been suggested to be a biochemical hallmark of seizure-induced neuronal cell death and epileptogenesis. Therefore, protection of mitochondria from bioenergetic failure and oxidative stress in the hippocampus may open a new vista to the development of effective neuroprotective strategies against seizure-induced brain damage and to the design of novel treatment perspectives against therapy-resistant forms of epilepsy.
癫痫被认为是全球最常见的神经障碍之一。与长时间癫痫放电相关的爆发性神经元放电可能导致大量变化，并在细胞水平上引发级联事件。线粒体不仅作为细胞的能量工厂，还在细胞死亡机制中发挥着关键作用。新出现的证据表明，长时间的癫痫发作可能导致线粒体功能障碍，增加海马区的氧化和硝化应激，从而导致神经元细胞死亡，并导致随后的癫痫发生。研究表明，线粒体呼吸链复合物 I 的选择性功能障碍是癫痫诱导的神经元细胞死亡和癫痫发生的生化特征。因此，保护海马体线粒体免受生物能量衰竭和氧化应激的影响，可能为开发针对癫痫引起的脑损伤的有效神经保护策略以及针对耐药性癫痫形式的新型治疗方法开辟新的前景。
