Neuroprotective Effect of Lycopene Against PTZ-induced Kindling Seizures in Mice: Possible Behavioural, Biochemical and Mitochondrial Dysfunction

Oxidative stress and mitochondrial dysfunction are the major contributing factors in the pathophysiology of various neurological disorders. Recently, antioxidant therapies aimed at reducing oxidative stress gained a considerable attention in epilepsy treatment. Lycopene, a carotenoid antioxidant, has received scientific interest in recent years. So, the present study has been designed to evaluate the neuroprotective effect of lycopene against the pentylenetetrazol (PTZ)-induced kindling epilepsy. Laca mice received lycopene (2.5, 5 and 10mg/kg) and sodium valproate for a period of 29days and PTZ (40mg/kg i.p (Intraperitoneal)) injection on alternative days. Various behavioural (kindling score), biochemical parameters (lipid peroxidation, superoxide dismutase, reduced glutathione, catalase and nitrite) and mitochondrial enzyme complex activities (I, II and IV) were assessed in the brain. Results depicted that repeated administration of a sub-convulsive dose of PTZ (40mg/kg) significantly increased kindling score, oxidative damage and impaired mitochondrial enzyme complex activities (I, II and IV) as compared with naive animals. Lycopene (5 and 10mg/kg) and sodium valproate (100mg/kg) treatment for a duration of 29days significantly attenuated kindling score, reversed oxidative damage and restored mitochondrial enzyme complex activities (I, II and IV) as compared with control. Thus, present study demonstrates the neuroprotective potential of lycopene in PTZ-induced kindling in mice. Copyright (c) 2015 John Wiley & Sons, Ltd.