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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 795259, 12 pages
Review Article

Oxidative Stress and Epilepsy: Literature Review

1School of Medicine, University of Fortaleza (UNIFOR)/RENORBIO, Rua Desembargador Floriano Benevides Magalhães, 221 3° Andar, 60811-690 Fortaleza, CE, Brazil
2Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Rua Coronel Nunes de Melo, 1127, 60430-270 Fortaleza, CE, Brazil
3School of Nursing, University of Fortaleza (UNIFOR)/RENORBIO, Avenida Washington Soares, 1321, 60811-905 Fortaleza, CE, Brazil
4School of Pharmacy, University of Otago, P.O. Box 913, Dunedin, New Zealand
5Pharmacy Department, Faculty of Dentistry, Nursing and Pharmacy, Federal University of Ceará, Rua Capitão Francisco Pedro, 1210, 60430-370 Fortaleza, CE, Brazil

Received 8 March 2012; Revised 7 May 2012; Accepted 24 May 2012

Academic Editor: Regina Menezes

Copyright © 2012 Carlos Clayton Torres Aguiar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy. Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed. Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.