Serum paraoxonase-1 activities and malondialdehyde levels in patients with epilepsy

Öz

Objectives: We aimed to evaluate antioxidant paraoxonase-1 (PON-1) activity together with malondialdehyde (MDA) (an oxidative stress parameter) levels in patients with epilepsy. Materials and methods: Forty-five epilepsy patients were included in the study and compared with healthy controls (n = 45). The levels of serum MDA and PON-1 activities were measured by the Ohkawa method and the Eckerson method, respectively. Results: Serum MDA level was significantly higher (P = 0.015), whereas PON-1 activity was sigificantly lower (P = 0.011) in the patient group than the controls. Conclusions: Increased reactive oxygen species levels in epilepsy may result in a oxidative stress, which in turn could result in decreased antioxidant PON-1 activity and increased MDA levels.

Anahtar Kelimeler

• Epilepsy, oxidative stress, malondialdehyde, paraoxonase-1

Epilepsili hastalarda serum paraoksonaz-1 aktivitesi ve malondialdehit düzeyleri

Öz

Amaç: Amacımız epilepsili hastalarda serumda antioksidan olarak paraoksonaz-1 (PON-1) aktivitesi ve malondialdehit (MDA) (oksidatif stres parametresi) düzeylerini değerlendirmektir.Gereç ve yöntem: Çalışmaya kırk beş epilepsi hastası alındı ve kontrol sağlıklı 45 kişi ile karşılaştırıldı. Serum MDA düzeyleri ve PON-1 aktiviteleri sırasıyla Ohkawa ve Eckerson metodları ile ölçüldü.Bulgular: Serum MDA seviyeleri hasta grubunda (3,97±0,71 nmol/mL) kontol grubuna (3,52±0,95 nmol/mL) göre anlamlı yüksek (p = 0,015) iken, PON-1 aktiviteleri hasta grubunda kontrol grubuna göre anlamlı düşük bulundu (45,17±29,70 U/L ve 66,50±46,15 U/L, p= 0,011).Sonuç: Epilepside reaktif oksijen türlerinin seviyelerinin artması oksidatif stresin bir sonucu olabilir. Bu sebeple antioksidan olarak PON-1 aktivitesi azalırken, MDA düzeyleri artabilir

Anahtar Kelimeler

• Epilepsi, oksidatif stres, malondialdehit, paraoksonaz-1

Kaynakça

1. Zupec-Kania BA, Spellman E. An overview of the ketogenic diet for pediatric epilepsy. Nutr Clin Pract 2008;23(6):589- 96.
2. Devi PU, Manocha A, Vohora D. Seizures, antiepileptics, an- tioxidants and oxidative stress: an insight for researchers. Exp Opin pharmacother 2008;9(18):3169-77.
3. Menon B, Ramalingam K, Kumar RV. Oxidative stress in patients with epilepsy is independent of antiepileptic drugs. Seizure 2012;21(10):780-4.
4. Perrone S, Negro S, Tataranno ML, et al. Oxidative stress and antioxidant strategies in newborns. J Maternal-Fetal Neo- nate 2010;23 Suppl 3:63-5.
5. Aguiar CC, Almeida AB, Araujo PV, et al. Oxidative stress and epilepsy: literature review. Oxid Med Cell Longevity 2012;2012:795259.
6. Giera M, Lingeman H, Niessen WM. Recent Advance- ments in the LC- and GC-Based Analysis of Malondi- aldehyde (MDA): A Brief Overview. Chromatographia 2012;75(9):433-40.
7. Schrader C, Ernst IM, Sinnecker H, et al. Genistein as a potential inducer of the anti-atherogenic enzyme paraox- onase-1: studies in cultured hepatocytes in vitro and in rat liver in vivo. J Cell Mol Med 2012;16(10):2331-41.
8. Draganov DI, La Du BN. Pharmacogenetics of paraoxonas- es: a brief review. Naunyn-Schmiedeberg’s Arch Pharma- col 2004; 369(1):78-88.

9. Berbecki J, Mitosek-Szewczyk K, Kurzepa J, et al. Processes of free radical lipid peroxidation with a particular regard to the role of paraoxonase-1 in the pathogenesis of multiple sclerosis. Wiad Lek 2011;64(1):31-6.
10. Baluchnejadmojarad T, Roghani M. Coenzyme Q10 ame- liorates neurodegeneration, mossy fiber sprouting, and oxi- dative stress in intrahippocampal kainate model of temporal lobe epilepsy in rat. J Mol Neurosci 2012 Sep 25. [Epub ahead of print].
11. Ohkawa H, Ohishi N, Tagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Bio- chem 1979; 95(2):351-8.
12. Eckerson HW, Romson J, Wyte C, et al. The human paraox- onase polymorphism: identification of phenotypes by their response to salts. Am J Hum Genet 1983;35(2):214-27.
13. Freitas RM. Investigation of oxidative stress involvement in hippocampus in epilepsy model induced by pilocarpine. Neuroscience Lett 2009;462(3):225-9.
14. Frantseva MV, Perez Velazquez JL, et al. Oxidative stress is involved in seizure-induced neurodegeneration in the kin- dling model of epilepsy. Neuroscience 2000;97(3):431-5.
15. Kutluhan S, Naziroglu M, Celik O, Yilmaz M. Effects of selenium and topiramate on lipid peroxidation and antioxi- dant vitamin levels in blood of pentylentetrazol-induced ep- ileptic rats. Biol Trace Element Res 2009;129(1-3):181-9.
16. Ramaekers VT, Bosman B, Jansen GA, et al. Increased plasma malondialdehyde associated with cerebellar struc- tural defects. Arch Dis Child 1997;77(3):231-4.
17. Peker E, Oktar S, Ari M, et al. Nitric oxide, lipid peroxida- tion, and antioxidant enzyme levels in epileptic children us- ing valproic acid. Brain Res 2009;1297(1):194-7.
18. Yildiz M, Simsek G, Uzun H, et al. Assessment of low-den- sity lipoprotein oxidation, paraoxonase activity, and arterial distensibility in epileptic children who were treated with anti-epileptic drugs. Cardiol Young 2010;20(5):547-54.
19. Karikas GA, Schulpis KH, Bartzeliotou A, et al. Early effects of sodium valproate monotherapy on serum para- oxonase/arylesterase activities. Scand J Clin Lab Invest 2009;69(1):31-5.
20. Cardenas-Rodriguez N, Coballase-Urrutia E, Huerta-Ger- trudis B, et al. Antioxidant activity of topiramate: An an- tiepileptic agent. Neurol Sci 2012 [Epub ahead of print].
21. Chaudhary S, Parvez S. An in vitro approach to assess the neurotoxicity of valproic acid-induced oxidative stress in cerebellum and cerebral cortex of young rats. Neuroscience 2012;225(3):258-68.