ORIGINAL ARTICLE Antioxidative–oxidative balance in epilepsy patients on antiepileptic therapy: a prospective case–control study Selda Keskin Guler 1 • Bilal Aytac 2 • Zahide Esra Durak 3 • Burcu Gokce Cokal 1 • Nalan Gunes 1 • Ilker Durak 4 • Tahir Yoldas 1 Received: 14 September 2015 / Accepted: 21 January 2016 Ó Springer-Verlag Italia 2016 Abstract Oxidative stress has been implicated in various disorders, including epilepsy. The aim of this study was to investigate the oxidant and antioxidant status of patients with epilepsy using antiepileptic drugs regularly and to compare them with healthy subjects. We investigated serum catalase (CAT), malondialdehyde (MDA), glu- tathione peroxidase (GSH-Px), superoxide dismutase (SOD), and xanthine oxidase (XO) levels in 58 epilepsy patients and 25 healthy controls. Patients were divided into polytherapy (n = 17) and monotherapy (n = 41) groups, and antioxidant status was compared between the two groups and controls. There was no significant difference between the patient and control groups in terms of age or gender (p [ 0.05). The mean duration of illness in the patients was 14.8 years, and the mean duration of treatment was 11.4 years. Comparison of the patient and control groups in terms of oxidative stress and antioxidant defence parameters revealed significantly higher MDA, GSH-Px, XO and lower level of CAT, SOD levels (p \ 0.05). There were no differences in CAT, MDA, GSH-Px or SOD levels between the monotherapy and polytherapy groups; but the XO level was higher in the monotherapy group (p \ 0.05). Although the XO level was decreased by polytherapy, it was higher than in controls. Our study found significantly low level of antioxidants in patients with epilepsy as compared to control. Thus, antiepileptic treatment did not improve oxidative stress parameters. Furthermore, our results show that polytherapy does not change the situation as compared with monotherapy. Antioxidant replacement therapy may benefit these patients. Keywords Oxidative balance Á Antioxidant effect Á Antiepileptic drugs Á Polytherapy Á Monotherapy Introduction Epilepsy is a fairly common chronic, complex neurological disease known since antiquity, and affects 1–3 % of the general population [1]. Defective ion transport or ion channel structure in the neuronal membrane, inhibitory–excitatory mechanisms, and regulatory modulator systems have been implicated in the pathogenesis of epilepsy [2–4]. In addition, impaired antioxidant defence mechanisms and increased lipid peroxidation are also implicated in its pathogenesis [5– 8]. The effects of antiepileptic medications in previous studies have paralleled these hypotheses. Two studies have suggested that the oxidant–antioxidant balance is regulated by antiepileptic therapy in epilepsy patients [8, 9]. In its simplest definition, oxidative stress refers to an imbalance between the body’s antioxidant defence capacity and free radical production as a result of peroxidation of the lipid layer of cells. Oxidative stress, as a possible mechanism of toxicity, has been the focus of many toxi- cological studies in the last decade. The abstract of this paper was presented at 31th International Epilepsy Congress in Istanbul, Turkey, at 5–9th September 2015. & Selda Keskin Guler keskinselda@gmail.com 1 Department of Adult Neurology, Ankara Training and Research Hospital, S ¸u ¨kriye District, Ulucanlar Avenue, No: 89, Altındag ˘, 06340 Ankara, Turkey 2 General Directorate of Health Information Systems, Ministry of Health, Ankara, Turkey 3 The Laboratory of Turkish Public Health Institution, Ministry of Health, Ankara, Turkey 4 Department of Biochemistry, Ankara University Faculty of Medicine, Ankara, Turkey 123 Neurol Sci DOI 10.1007/s10072-016-2494-0