School of Medicine, University of Fortaleza/RENORBIO, Rua Desembargador Floriano Benevides Magalhães, 221 3° Andar, 60811-690 Fortaleza, CE, Brazil.
Oxid Med Cell Longev. 2012;2012:795259. doi: 10.1155/2012/795259. Epub 2012 Jul 14.
The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy.
A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed.
RESULTS/CONCLUSIONS: Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.
自由基的产生在生物功能调节、细胞损伤和中枢神经系统疾病发病机制中发挥作用。癫痫是一种高发的严重脑部疾病，氧化应激被认为是癫痫发生的可能机制之一。实验研究表明，氧化应激是癫痫发作和演变的一个促成因素。
对氧化应激与癫痫发作、氧化应激与年龄作为癫痫发病风险因素之间的关系进行综述。同时探讨氧化应激在癫痫发作诱导和传播中的作用。
结果/结论：氧化应激和线粒体功能障碍与神经元死亡和癫痫发作有关。有证据表明，抗氧化治疗可能会减少一些动物癫痫模型中氧化自由基诱导的损伤。研究表明，线粒体功能障碍与慢性氧化应激有关，可能在癫痫发生过程中发挥重要作用；但是，很少有研究表明氧化应激、癫痫发作和年龄之间存在明确的联系。
