الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Epilepsy is one of the most common neurological disorders worldwide. Epilepsy is diagnosed after a patient has two or more unprovoked seizures.
Epilepsy is a potentially life-threatening condition and is associated with increased mortality particularly in patients with chronic epilepsy. Possible causes of death include a complication of epilepsy, e.g. trauma, aspiration of gastric content, convulsive status epilepticus, a complication of drug treatment or a related underlying cause.
Oxidative stress usually results from either increasing oxidant enzymes or decreasing antioxidant enzymes and results in excessive levels of free radical intermediates.
The oxidant/antioxidant balance in epilepsy is not only modulated by seizures per se, The metabolism of valproic acid may trigger oxygen dependent tissue injury and elevate the free radicals in the body. Furthermore, valproic acid enhances the clearance of zinc, copper and selenium, subsequently leading to decreased synthesis of free radicals scavenging enzymes as glutathione peroxidase and glutathione reductase activities.
Carbamazepine decrease levels of antioxidant enzymes especially glutathione peroxidase and catalase in erythrocytes and decrease glutathione level which is a cofactor of several enzymes against oxidative stress.
The present study was designed to assess DNA damage in epileptic patients treated with Valproic Acid or Carbamazepine monotherapy and to relate it to different clinical features of the patients.