FREE RADICALS, EPILEPSY AND ANTI-OXIDANT: AN OVERVIEW

Abstract

Epilepsy is a common and heterogeneous disorder arising from biochemical and molecular events in the brain that are incompletely understood. Oxidative stress is emerging as a mechanism that may play an important role in the etiology of seizure induced neuronal death. In oxidative stress generation the free radical called reactive oxygen species and reactive nitrogen species (ROS, RNS) result in oxidative damage to cellular protein lipid and DNA and contribute the majority of seizure induced free radical prediction. Episodes of seizures can be prevented by eliminating causative or precipitating factors. However, the use of an antioxidant is a redox active compound that limits oxidative stress by reacting nonenzymatically with a reactive oxidant. Although oxidation reactions are critical for life, they can also be damaging; hence, plants and animals maintain complex systems of multiple types of antioxidants, such as glutathione, vitamin C, and vitamin E as well as enzymes such as catalase, superoxide dismutase and various peroxidase. Melatonin is one of the major antioxidant which is an pineal hormone, acts as a direct free radical scavenger and indirect antioxidant. It is suggested that the increase in neurodegenerative diseases is most prominent reason for decrease in the levels of melatonin with age. Unlike other antioxidants, melatonin can easily cross all morphophysiological barriers and enter in cell compartments. Evidence are accumulating to suggest the potential of melatonin in neurodegenerative conditions, but much information needs to be generated before it find place as a drug on the treatment of epilepsy.