氧化应激
脂质过氧化
癫痫
癫痫发生
神经退行性变
药理学
抗氧化剂
褪黑素
谷胱甘肽
神经保护
化学
维生素E
医学
生物化学
内科学
神经科学
生物
酶
疾病
作者
Krzysztof Łukawski,Stanisław J. Czuczwar
出处
期刊:Antioxidants
[MDPI AG]
日期:2023-05-05
卷期号:12 (5): 1049-1049
被引量:2
标识
DOI:10.3390/antiox12051049
摘要
Free radicals are generated in the brain, as well as in other organs, and their production is proportional to the brain activity. Due to its low antioxidant capacity, the brain is particularly sensitive to free radical damage, which may affect lipids, nucleic acids, and proteins. The available evidence clearly points to a role for oxidative stress in neuronal death and pathophysiology of epileptogenesis and epilepsy. The present review is devoted to the generation of free radicals in some animal models of seizures and epilepsy and the consequences of oxidative stress, such as DNA or mitochondrial damage leading to neurodegeneration. Additionally, antioxidant properties of antiepileptic (antiseizure) drugs and a possible use of antioxidant drugs or compounds in patients with epilepsy are reviewed. In numerous seizure models, the brain concentration of free radicals was significantly elevated. Some antiepileptic drugs may inhibit these effects; for example, valproate reduced the increase in brain malondialdehyde (a marker of lipid peroxidation) concentration induced by electroconvulsions. In the pentylenetetrazol model, valproate prevented the reduced glutathione concentration and an increase in brain lipid peroxidation products. The scarce clinical data indicate that some antioxidants (melatonin, selenium, vitamin E) may be recommended as adjuvants for patients with drug-resistant epilepsy.
科研通智能强力驱动
Strongly Powered by AbleSci AI