Oxidative stress, mitochondrial dysfunction, and epilepsy.
Epilepsy is a common and heterogeneous neurological disorder arising from biochemical and molecular events that are incompletely understood. To effectively manage epilepsies, it is important to understand the mechanisms underlying both seizure-induced brain damage as well as seizure initiation. Oxidative stress is emerging as a mechanism that may play an important role in the etiology of seizure-induced neuronal death. Conversely, epileptic seizures are a common occurrence in mitochondrial diseases arising from defects in oxidative phosphorylation. This review focuses on the emerging role of oxidative stress and mitochondrial dysfunction both as a consequence and cause of epileptic seizures.
Patel
Manisha N
MN
National Jewish Medical and Research Center and University of Colorado Health Sciences Center, 1400 Jackson Street, Room K706, Denver, CO 80206, USA. patelm@njc.org
D004272:DNA, Mitochondrial / Q000378:metabolism; D004827:Epilepsy / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D028361:Mitochondrial Diseases / Q000378:metabolism / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species
D004272:DNA, Mitochondrial; D017382:Reactive Oxygen Species; D009569:Nitric Oxide