Neuronal oxidative injury in the development of the epileptic disease : a potential target for novel therapeutic approaches

Abstract

Epileptic diseases affect about 50 million people in the world and approximately 30% of patients diagnosed with epilepsy are unresponsive to current medications. For these reasons, primary prevention of epilepsy represents one of the priorities in epilepsy research. Intracellular oxido-reductive (redox) state is well known to play a crucial role, contributing to the maintenance of the proper function of biomolecules. Therefore, oxidative stress results in functional cellular disruption and cellular damage and may cause subsequent cell death via oxidation of proteins, lipids, and nucleotides. Recently, the role of oxidative stress in the early stage and in the progression of epileptic disorders has begun to be recognized. The early molecular response to oxidative stress represents a short-term reversible phenomenon that precedes higher and irreversible forms of oxidation. This article reviews the current understanding of the epileptogenic phenomena related to seizure-induced oxidative injury as potential “critical period” therapeutic targets for the prevention of chronic epileptic disorder.