Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid

Peker, Erdal; Oktar, Süleyman; Arı, Mustafa; Kozan, Ramazan; Doğan, Murat; Çağan, Eren; Söğüt, Sadık

doi:10.1016/j.brainres.2009.08.048

Cited by 34 publications

(25 citation statements)

References 26 publications

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“…In this context, we observed no altered oxidative status in patients affected by idiopathic epilepsy syndromes under chronic VPA monotherapy. The latter data, which are congruent with what was observed in some previous studies [26,35], clearly suggest that the VPA may not be responsible of the altered oxidative status observed in Group 1 patients (81% of them was under VPA therapy). However, the relationship between chronic assumption of AEDs and oxidative stress needs to be clarified.…”

Section: Discussionsupporting

confidence: 91%

Oxidative stress in children affected by epileptic encephalopathies

Grosso¹,

Longini²,

Rodriguez³

et al. 2011

Journal of the Neurological Sciences

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Section: Discussionsupporting

confidence: 91%

Oxidative stress in children affected by epileptic encephalopathies

Grosso¹,

Longini²,

Rodriguez³

et al. 2011

Journal of the Neurological Sciences

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“…There are limited studies about CAT activities in VPA treatment. Peker et al 55 found no difference in serum CAT activities in children receiving VPA. In this study, CAT activities also did not change in the VPA group.…”

Section: Discussionmentioning

confidence: 93%

Edaravone ameliorates the adverse effects of valproic acid toxicity in small intestine

et al. 2014

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Valproic acid (VPA) is a drug used for the treatment of epilepsy, bipolar psychiatric disorders, and migraine. Previous studies have reported an increased generation of reactive oxygen species and oxidative stress in the toxic mechanism of VPA. Edaravone, a free radical scavenger for clinical use, can quench free radical reaction by trapping a variety of free radical species. In this study, effect of edaravone on some small intestine biochemical parameters in VPA-induced toxicity was investigated. Thirty seven Sprague Dawley female rats were randomly divided into four groups. The groups include control group, edaravone (30 mg–1 kg–1 day–1) given group, VPA (0.5 g–1 kg–1 day–1) given group, VPA + edaravone (in same dose) given group. Edaravone and VPA were given intraperitoneally for 7 days. Biochemical parameters such as malondialdehyde, as an index of lipid peroxidation(LPO), sialic acid (SA), glutathione levels and glutathione peroxidase, glutathione- S-transferase, superoxide dismutase, catalase, myeloperoxidase, alkaline phosphatase (ALP), and tissue factor (TF) activities were determined in small intestine samples by colorimetric methods. Decreased small intestine antioxidant enzyme activities, increased LPO and SA levels, and increased activities of ALP and TF were detected in the VPA group. Based on our results edaravone may be suggested to reverse the oxidative stress and inflammation due to VPA-induced small intestine toxicity.

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“…Extracellular SOD represents a major defense system against superoxide, being also a target for oxidative damage (36). Previous studies on SOD activity have mainly been performed in children with epilepsy on different AEDs, but they reported no significant difference in SOD activity between children with epilepsy and controls (1,10,37,38). Recently, Yis et al (39) have found a positive correlation between SOD activity and duration of valproic acid treatment in children with epilepsy.…”

Section: Discussionmentioning

confidence: 99%

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

Ercegovac¹,

Jović²,

Simić³

et al. 2013

Journal of Medical Biochemistry

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List of abbreviations: AEDs -antiepileptic drugs, 8 -epi-PGF 2a -urinary isoprostanes, GPX -glutathione peroxidase, ILAE -International League Against Epilepsy, 8-OHdG -8-hydroxy-2'-deoxyguanosine, P-SH -protein thiol groups, RCD -reactive carbonyl derivatives, ROS -reactive oxygen species, SOD -superoxide dismutase. SummaryBackground: To get more insight into the effects of the most widely used antiepileptic drugs (AEDs) on the pro oxi dant/ antioxidant balance in epi lep sy, a comparative analysis of the byproducts of oxidative damage and antioxidant de fense mechanisms was performed in patients with epilepsy treated with la mo trigine, carbamazepine and valproic acid. Methods: Byproducts of oxidative damage to proteins (reactive carbonyl derivatives, RCD and protein thiol groups, P-SH), lipids (urinary isoprostanes, 8 -epi-PGF 2a ) 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-PGF 2a 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-PGF 2a and 8-

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Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid

Cited by 34 publications

References 26 publications

Oxidative stress in children affected by epileptic encephalopathies

Oxidative stress in children affected by epileptic encephalopathies

Edaravone ameliorates the adverse effects of valproic acid toxicity in small intestine

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

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