Oxidative stress damage to mitochondria mediated the pathological processes in epilepsy

Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti-oxygen system. Mitochondrium is crucial to sustaining energy metabolism, regulating cell death, synthesising neurotransmitter and oxidating fatty acid. Mitochondrium is not only the place for free radical production, but also the target of oxidative damage. Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility. Seizure-induced free radical can influence energy metabolism, destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy.