Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Physiol Res. 2013;62(Suppl 1):S39-48. doi: 10.33549/physiolres.932613.
The existing data indicate that status epilepticus (SE) induced in immature animals is associated with oxidative stress and mitochondrial dysfunction. This has been demonstrated using two models of SE, induced by substances with a different mechanism of action (DL-homocysteic acid and 4-aminopyridine) which suggests that the findings are not model-dependent but they reflect more general phenomenon. Oxidative stress occurring in immature brain during and following seizures is apparently due to both the increased free radicals production and the limited antioxidant defense. Pronounced inhibition of mitochondrial complex I in immature brain was demonstrated not only during the acute phase of SE, but it persisted during long periods of survival, corresponding to the development of spontaneous seizures (epileptogenesis). The findings suggest that oxidative modification is most likely responsible for the sustained deficiency of complex I activity. It can be assumed that the substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment of epilepsy.
现有数据表明，在发育不成熟的动物中诱导的癫痫持续状态（SE）与氧化应激和线粒体功能障碍有关。这已通过两种 SE 模型得到证实，这两种模型是由作用机制不同的物质（DL-同型半胱氨酸和 4-氨基吡啶）诱导的，这表明这些发现不是依赖于模型的，而是反映了更普遍的现象。在癫痫发作期间和之后，发育中大脑中的氧化应激显然是由于自由基产生增加和抗氧化防御有限所致。在 SE 的急性阶段，不仅在成熟的大脑中观察到线粒体复合物 I 的明显抑制，而且在长时间的存活期间，即自发发作（癫痫发生）期间，也持续存在这种抑制。这些发现表明，氧化修饰很可能是导致复合物 I 活性持续缺乏的原因。可以假设，具有抗氧化特性的物质与常规疗法相结合可能对癫痫的治疗有有益的效果。
