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.
Highlights
The important role of oxidative stress and reactive oxygen species (ROS) in seizure disorders has emerged in the last decade [1,2,3,4]
The results of this study have shown that treatments with lamotrigine, carbamazepine and valproic acid affect the prooxidant/antioxidant balance in patients with epilepsy
It has been reported that increased generation of free radicals or reduced activity of antioxidative defense mechanisms can cause some forms of epilepsy and, in addition, increases the risk of seizure recurrence [2, 5,6,7]
Summary
The important role of oxidative stress and reactive oxygen species (ROS) in seizure disorders has emerged in the last decade [1,2,3,4]. It has been shown that long-term use of AEDs, such as carbamazepine, phenobarbital or valproic acid, increases free radical formation and causes oxidative damage within neuronal cells [6, 15, 16]. It remains unclear whether the prooxidant challenge of AEDs is associated with significant adverse effects on the antioxidant defense system, since major antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPX), have been reported to be increased, unchanged or decreased [1, 2, 7, 14]
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