Metabolic Dysfunction and Oxidative Stress in Epilepsy

被引:191
|
作者
Pearson-Smith, Jennifer N. [1 ]
Patel, Manisha [1 ]
机构
[1] Univ Colorado, Dept Pharmaceut Sci, Anschutz Med Campus, Aurora, CO 80045 USA
来源
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2017年 / 18卷 / 11期
关键词
mitochondria; reactive oxygen species; seizures; MITOCHONDRIAL COMPLEX-I; PROGRESSIVE NEURONAL DEGENERATION; SUPEROXIDE-PRODUCTION; NADPH OXIDASE; DRAVET SYNDROME; KETOGENIC DIET; CELL-DEATH; GLUTATHIONE-PEROXIDASE; NA+; K+-ATPASE ACTIVITY; STATUS EPILEPTICUS;
D O I
10.3390/ijms18112365
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The epilepsies are a heterogeneous group of disorders characterized by the propensity to experience spontaneous recurrent seizures. Epilepsies can be genetic or acquired, and the underlying mechanisms of seizure initiation, seizure propagation, and comorbid conditions are incompletely understood. Metabolic changes including the production of reactive species are known to result from prolonged seizures and may also contribute to epilepsy development. In this review, we focus on the evidence that metabolic and redox disruption is both cause and consequence of epileptic seizures. Additionally, we discuss the promise of targeting redox processes as a therapeutic option in epilepsy.
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页数:13
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