ABSTRACT
It is evident that oxidative stress plays an important role in epilepsy. Existing ndings indicate that reactive oxygen and/or nitrogen species (ROS and RNS) are involved in seizure-induced brain injury and lead to mitochondrial dysfunction, evident particularly as a marked inhibition of respiratory chain complex I, detected both in humans and in several models of epilepsy in adult and immature animals. Other targets sensitive to oxidative damage are DNA, particularly mitochondrial DNA (mtDNA), and phospholipids of biological membranes. Oxidative stress also substantially affects the properties of the neurovascular unit, increases the permeability of the blood-brain barrier, and alters the regulation of regional cerebral blood ow. The ndings suggest that the redox status shifts to a more oxidized state and the persisting oxidized environment may favor oxidative posttranslational modications of sensitive targets. The selected ROS and/or RNS scavengers have been shown to prevent or at least substantially attenuate seizure-induced ROS production, mitochondrial dysfunction, and brain injury associated with status epilepticus.
