Oxidative stress, mitochondrial dysfunction, and epilepsy

Free Radic Res. 2002 Nov;36(11):1139-46. doi: 10.1080/1071576021000016391.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • DNA, Mitochondrial / metabolism
  • Epilepsy / metabolism
  • Epilepsy / physiopathology*
  • Humans
  • Mitochondrial Diseases / metabolism
  • Mitochondrial Diseases / physiopathology*
  • Nitric Oxide / metabolism
  • Oxidative Stress / physiology*
  • Reactive Oxygen Species

Substances

  • DNA, Mitochondrial
  • Reactive Oxygen Species
  • Nitric Oxide