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Antiepileptic Drugs Affect Protein, Lipid and DNA Oxidative Damage and Antioxidant Defense in Patients with Epilepsy

M. Ercegovac,N. Jovic,T. Simić,L. Beslać-Bumbaširević,D. Sokić,A. Savić-Radojević,M. Matić,D. Jovanović,A. Ristić,Tatjana Đukić,S. Šuvakov,V. Ćorić,J. Mimic-oka,M. Plješa-Ercegovac

Published 2013 in Unknown venue

ABSTRACT

Summary Background: To get more insight into the effects of the most widely used antiepileptic drugs (AEDs) on the prooxidant/ antioxidant balance in epilepsy, a comparative analysis of the byproducts of oxidative damage and antioxidant de fense mechanisms was performed in patients with epilepsy treated with lamotrigine, carbamazepine and valproic acid. Methods: Byproducts of oxidative damage to proteins (reactive carbonyl derivatives, RCD and protein thiol groups, PSH), lipids (urinary isoprostanes, 8-epi-PGF2a) and DNA (urinary 8-hydroxy-2’-deoxyguanosine, 8-OHdG), as well as the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured in 60 patients with newly diagnosed seizure (at illness onset and after 6 months of treatment with lamotrigine, carbamazepine or valproic acid) and in 20 healthy controls. Results: In patients with epilepsy, RCD, urinary 8-epi-PGF2a and 8-OHdG, together with SOD and GPX activities were significantly increased, while P-SH were only slightly decreased. After 6 months of treatment with AEDs, a decrease was observed in RCD, urinary 8-epi-PGF2a and 8-OHdG to values slightly higher or similar to the control, while P-SH remained unchanged. A decrease was also observed in SOD and GPX activities, although they remained significantly in creased compared to controls. Conclusions: The results of this study have shown that treatments with lamotrigine, carbamazepine and valproic acid affect the prooxidant/antioxidant balance in patients with epilepsy. Kratak sadržaj Uvod: U pokušaju da se razjasne mehanizmi kojima naj cesce korisceni antiepilepticki lekovi (AEL) uticu na ravnotezu izmedu pro- i antioksidanasa u epilepsiji, u ovom radu je izvedena uporedna analiza pokazatelja oksidativnog o{te}enja i anti oksidantnih mehanizama za{tite kod bolesnika sa epilepsijom na terapiji lamotriginom, karbamazepinom ili valproi~ - nom kiselinom. Metode: Pokazatelji oksidativnog o{te}enja proteina (sa dr`aj karbonilnih grupa, RCD i koncentracija proteinskih tiol grupa plaz me, P-SH), lipida (urinarni izoprostani, 8-epi-PGF2a) i DNK (urinarni deoksiguanozin, 8-OHdG), kao i aktivnost anti oksidantnih enzima, superoksid dizmutaze (SOD) i glutation peroksidaze (GPX) odre|ivani su kod 60 bolesnika sa novo dijagnostikovanom epilepsijom (nakon prvog napada i posle 6 meseci, na terapiji lamotriginom, karbamazepinom ili valproi~nom kiselinom) i kod 20 zdravih osoba. Rezultati: Kod bolesnika sa epilepsijom, koncentracija RCD, 8-epi-PGF2a i 8-OHdG, kao i aktivnosti SOD i GPX su zna~ajno pove}ane, dok je koncentracija P-SH umereno smanjena. Nakon {estomese~ne terapije AEL, uo~eno je smanjenje koncentracije RCD, 8-epi-PGF2a i 8-OHdG do vrednosti sli~nih onim u kontrolnoj grupi, dok je koncentracija P-SH ostala neizmenjena. Zna~ajno smanjenje je uo~eno i u aktiv nosti SOD i GPX, mada vrednosti ostaju zna~ajno pove}ane u odnosu na kontrolu. Zaključak: Terapija lamotriginom, karbamazepinom i valproicnom kiselinom uti~e na ravnote`u izme|u prooksidanasa i antioksidanasa kod bolesnika sa epilepsijom.

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