<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">phkinetica</journal-id><journal-title-group><journal-title xml:lang="ru">Фармакокинетика и Фармакодинамика</journal-title><trans-title-group xml:lang="en"><trans-title>Pharmacokinetics and Pharmacodynamics</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2587-7836</issn><issn pub-type="epub">2686-8830</issn><publisher><publisher-name>ООО «Издательство ОКИ»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.37489/2587-7836-2022-2-11-16</article-id><article-id custom-type="elpub" pub-id-type="custom">phkinetica-313</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ИССЛЕДОВАНИЯ МЕХАНИЗМА ДЕЙСТВИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>MECHANISM OF ACTION RESEARCH</subject></subj-group></article-categories><title-group><article-title>Влияние максимального электрошока и противосудорожных препаратов на концентрацию продуктов перекисного окисления липидов в эксперименте на мышах</article-title><trans-title-group xml:lang="en"><trans-title>The effect of maximal electroshock seizure and anticonvulsants on the concentration of lipid peroxidation products in an experiment in mice</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8056-4142</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гайдуков</surname><given-names>И. О.</given-names></name><name name-style="western" xml:lang="en"><surname>Gaydukov</surname><given-names>I. O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Гайдуков Игорь Олегович, к. б. н., с. н. с. лаборатории психофармакологии</p><p>Москва</p></bio><bio xml:lang="en"><p>Gaydukov Igor O., PhD Biological Sci., Senior researcher of laboratory psychopharmacology</p><p>Moscow</p></bio><email xlink:type="simple">gaidukov01@rambler.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9139-2334</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Литвинова</surname><given-names>С. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Litvinova</surname><given-names>S. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Литвинова Светлана Александровна, к. б. н., в. н. с. лаборатории психофармакологии</p><p>Москва</p></bio><bio xml:lang="en"><p>Litvinova Svetlana A., PhD Biological Sci., Leading researcher Laboratory of Psychopharmacology</p><p>Moscow</p></bio><email xlink:type="simple">sa_litvinova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3528-4659</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Золотов</surname><given-names>Н. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Zolotov</surname><given-names>N. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Золотов Николай Николаевич, д. б. н., профессор, гл. н. с, лаборатории психофармакологии</p><p>Москва</p></bio><bio xml:lang="en"><p>Zolotov Nikolay N., Dr. Sci. Biological, professor, Chief researcher of laboratory psychopharmacology</p><p>Moscow</p></bio><email xlink:type="simple">zolotovnn@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7083-5298</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Котельникова</surname><given-names>С. О.</given-names></name><name name-style="western" xml:lang="en"><surname>Kotelnikova</surname><given-names>S. O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Котельникова Светлана Олеговна, к. б. н., с. н. с. лаборатории психофармакологии</p><p>Москва</p></bio><bio xml:lang="en"><p>Kotelnikova Svetlana O., PhD Biological Sci., Senior researcher, laboratory of psychopharmacology</p><p>Moscow</p></bio><email xlink:type="simple">ailantha@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3566-6203</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воронина</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Voronina</surname><given-names>T. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Воронина Татьяна Александровна, д. м. н., профессор, руководитель лаборатории психофармакологии. SPIN-код: 5766-3452</p><p>Москва</p></bio><bio xml:lang="en"><p>Voronina Tatiana A., Dr. Sci. (Med.), professor, Head Laboratory of psychopharmacology. SPIN code: 5766-3452</p><p>Moscow</p></bio><email xlink:type="simple">voroninata38@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «НИИ фармакологии имени В.В. Закусова»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>FSBI “Zakusov Institute of Pharmacology”</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>06</day><month>07</month><year>2022</year></pub-date><volume>0</volume><issue>2</issue><fpage>11</fpage><lpage>16</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Гайдуков И.О., Литвинова С.А., Золотов Н.Н., Котельникова С.О., Воронина Т.А., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Гайдуков И.О., Литвинова С.А., Золотов Н.Н., Котельникова С.О., Воронина Т.А.</copyright-holder><copyright-holder xml:lang="en">Gaydukov I.O., Litvinova S.A., Zolotov N.N., Kotelnikova S.O., Voronina T.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.pharmacokinetica.ru/jour/article/view/313">https://www.pharmacokinetica.ru/jour/article/view/313</self-uri><abstract><p>Окислительный стресс играет одну из ключевых ролей в эпилептогенезе. Целью исследования было оценить влияние судорог на развитие оксидативного стресса и наличие антиоксидантных свойств у карбамазепина и вальпроевой кислоты при судорожном состоянии, вызванном максимальным электрошоком (МЭШ). Методы. У мышей вызывали электросудорожные припадки методом МЭШ с оценкой тяжести судорог по балльной шкале. Оценку оксидативного стресса проводили по продуктам перекисного окисления липидов (ПОЛ), определяемых в плазме крови. Результаты. Установлено, что воздействие МЭШ с последующими тонико-клоническими припадками приводит к оксидативному стрессу у мышей. Вальпроевая кислота и карбамазепин полностью защищали от возникновения судорог после воздействия МЭШ, однако концентрация продуктов ПОЛ не отличалась от группы с МЭШ и была также выше, чем в группе контроля.</p></abstract><trans-abstract xml:lang="en"><p>Oxidative stress plays a key role in epileptogenesis. The aim of the study was to evaluate the effect of seizures on the development of oxidative stress and the presence of antioxidant properties in carbamazepine and valproic acid in convulsive state caused by maximal electroshock seizure (MES). Methods. An electroconvulsive seizure were induced by the MES-test in mice, with assessment of the severity of seizures on a point scale. Oxidative stress was assessed by products of lipid peroxidation (LPO) determined in blood plasma. Results. It has been established that exposure to MES followed by tonic-clonic seizures leads to oxidative stress in mice. Valproic acid and carbamazepine completely protected against seizures after MES-test, however, the concentration of lipid peroxidation products did not differ from the MES group and was also higher than in the control group.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>МЭШ</kwd><kwd>карбамазепин</kwd><kwd>вальпроевая кислота</kwd><kwd>окислительный стресс</kwd><kwd>ПОЛ</kwd><kwd>ТБК-активные продукты</kwd></kwd-group><kwd-group xml:lang="en"><kwd>MES</kwd><kwd>carbamazepine</kwd><kwd>valproic acid</kwd><kwd>oxidative stress</kwd><kwd>lipid peroxidation</kwd><kwd>TBA-active products</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Aguiar СС, Almeida АВ, Araújo PV, de Abreu RN, et al. Oxidative stress and epilepsy: literature review. Oxid Med Cellr Longev. 2012;2012:795259. DOI: 10.1155/2012/795259.</mixed-citation><mixed-citation xml:lang="en">Aguiar СС, Almeida АВ, Araújo PV, de Abreu RN, et al. Oxidative stress and epilepsy: literature review. Oxid Med Cellr Longev. 2012;2012:795259. DOI: 10.1155/2012/795259.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Ferriero DM. Protecting neurons. Epilepsia. 2005;46(7):45–51. DOI: 10.1111/j.1528-1167.2005.00302.x.</mixed-citation><mixed-citation xml:lang="en">Ferriero DM. Protecting neurons. Epilepsia. 2005;46(7):45–51. DOI: 10.1111/j.1528-1167.2005.00302.x.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Beltrán-Sarmiento E, Arregoitia-Sarabia CK, Floriano-Sánchez E, et al. Effects of valproate monotherapy on the oxidant-antioxidant status in mexican epileptic children: a longitudinal study. Oxid Med Cellr Longev. 2018;2018:7954371. DOI: 10.1155/2018/7954371.</mixed-citation><mixed-citation xml:lang="en">Beltrán-Sarmiento E, Arregoitia-Sarabia CK, Floriano-Sánchez E, et al. Effects of valproate monotherapy on the oxidant-antioxidant status in mexican epileptic children: a longitudinal study. Oxid Med Cellr Longev. 2018;2018:7954371. DOI: 10.1155/2018/7954371.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Yuksel A, Cengiz, M, Seven M, et al. Erythrocyte glutathione, glutathione peroxidase, superoxide dismutase and serum lipid peroxidation in epileptic children with valproate and carbamazepine monotherapy. J Basic Clin Physiol Pharmacol. 2000;11(1):73–81. DOI: 10.1515/jbcpp.2000.11.1.73.</mixed-citation><mixed-citation xml:lang="en">Yuksel A, Cengiz, M, Seven M, et al. Erythrocyte glutathione, glutathione peroxidase, superoxide dismutase and serum lipid peroxidation in epileptic children with valproate and carbamazepine monotherapy. J Basic Clin Physiol Pharmacol. 2000;11(1):73–81. DOI: 10.1515/jbcpp.2000.11.1.73.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Verrotti, A, Basciani F, Trotta D, et al. Serum copper, zinc, selenium, glutathione peroxidase and superoxide dismutase levels in epileptic children before and after 1 year of sodium valproate and carbamazepine therapy. Epilepsy Res. 2002;48(1-2):71–75. DOI: 10.1016/s0920-1211(01)00322-9.</mixed-citation><mixed-citation xml:lang="en">Verrotti, A, Basciani F, Trotta D, et al. Serum copper, zinc, selenium, glutathione peroxidase and superoxide dismutase levels in epileptic children before and after 1 year of sodium valproate and carbamazepine therapy. Epilepsy Res. 2002;48(1-2):71–75. DOI: 10.1016/s0920-1211(01)00322-9.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Liu CS, Wu HM, Kao SH, et al. Serum trace elements, glutathione, copper/zinc superoxide dismutase, and lipid peroxidation in epileptic patients with phenytoin or carbamazepine monotherapy. Clin Neuropharmacol. 1998;21(1):62–64.</mixed-citation><mixed-citation xml:lang="en">Liu CS, Wu HM, Kao SH, et al. Serum trace elements, glutathione, copper/zinc superoxide dismutase, and lipid peroxidation in epileptic patients with phenytoin or carbamazepine monotherapy. Clin Neuropharmacol. 1998;21(1):62–64.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Aycicek A., Iscan A. The effects of carbamazepine, valproic acid and phenobarbital on the oxidative and antioxidative balance in epileptic children. Eur Neurol. 2007;57(2):65–69. DOI: 10.1159/000098053.</mixed-citation><mixed-citation xml:lang="en">Aycicek A., Iscan A. The effects of carbamazepine, valproic acid and phenobarbital on the oxidative and antioxidative balance in epileptic children. Eur Neurol. 2007;57(2):65–69. DOI: 10.1159/000098053.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Higuchi S, Yano A, Takai S, et al. Metabolic activation and inflammation reactions involved in carbamazepine-induced liver injury. Toxicol Sci. 2012;130(1):4–16. DOI: 10.1093/toxsci/kfs222.</mixed-citation><mixed-citation xml:lang="en">Higuchi S, Yano A, Takai S, et al. Metabolic activation and inflammation reactions involved in carbamazepine-induced liver injury. Toxicol Sci. 2012;130(1):4–16. DOI: 10.1093/toxsci/kfs222.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Lu W, Uetrecht JP. Peroxidase-mediated bioactivation of hydroxylated metabolites of carbamazepine and phenytoin. Drug Metab Dispos. 2008;36(8):1624–1636. DOI: 10.1124/dmd.107.019554.</mixed-citation><mixed-citation xml:lang="en">Lu W, Uetrecht JP. Peroxidase-mediated bioactivation of hydroxylated metabolites of carbamazepine and phenytoin. Drug Metab Dispos. 2008;36(8):1624–1636. DOI: 10.1124/dmd.107.019554.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Brault S, Martinez-Bermudez AK, Marrache AM, et al. Selective Neuromicrovascular Endothelial Cell Death by 8-Iso-Prostaglandin F2: Possible Role in Ischemic Brain Injury. Stroke. 2003;34(3):776–782. DOI: 10.1161/01.STR.0000055763.76479.E6.</mixed-citation><mixed-citation xml:lang="en">Brault S, Martinez-Bermudez AK, Marrache AM, et al. Selective Neuromicrovascular Endothelial Cell Death by 8-Iso-Prostaglandin F2: Possible Role in Ischemic Brain Injury. Stroke. 2003;34(3):776–782. DOI: 10.1161/01.STR.0000055763.76479.E6.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Cam Ha TT, Antis GG, G. Campbell T, et al. Seizures elevate gliovascular unit Ca 2+ and cause sustained vasoconstriction. JCI Insight. 2020;5(19):e136469. DOI: 10.1172/jci.insight.136469.</mixed-citation><mixed-citation xml:lang="en">Cam Ha TT, Antis GG, G. Campbell T, et al. Seizures elevate gliovascular unit Ca 2+ and cause sustained vasoconstriction. JCI Insight. 2020;5(19):e136469. DOI: 10.1172/jci.insight.136469.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Van Den Pol AN, Obrietan K., Belousov A. Glutamate hyperexcitability and seizure-like activity throughout the brain and spinal cord upon relief from chronic glutamate receptor blockade in culture. Neuroscience. 1996;74(3):653–674. DOI: 10.1016/0306-4522(96)00153-4.</mixed-citation><mixed-citation xml:lang="en">Van Den Pol AN, Obrietan K., Belousov A. Glutamate hyperexcitability and seizure-like activity throughout the brain and spinal cord upon relief from chronic glutamate receptor blockade in culture. Neuroscience. 1996;74(3):653–674. DOI: 10.1016/0306-4522(96)00153-4.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Francisco JC, Hayley AM, Waldo C. Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies. Neural Plast. 2016;(2016):2701526. DOI: 10.1155/2016/2701526.</mixed-citation><mixed-citation xml:lang="en">Francisco JC, Hayley AM, Waldo C. Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies. Neural Plast. 2016;(2016):2701526. DOI: 10.1155/2016/2701526.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Halliwell B. Reactive oxygen species and the central nervous system. J Neurochem. 1992;59(5):1609–1623. DOI: 10.1111/j.1471-4159.1992.tb10990.x.</mixed-citation><mixed-citation xml:lang="en">Halliwell B. Reactive oxygen species and the central nervous system. J Neurochem. 1992;59(5):1609–1623. DOI: 10.1111/j.1471-4159.1992.tb10990.x.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Halliwell B, Gutteridge JMC. Free Radicals in Biology and Medicine. 3rd ed. Oxford: Oxford Univ. Press; 1999</mixed-citation><mixed-citation xml:lang="en">Halliwell B, Gutteridge JMC. Free Radicals in Biology and Medicine. 3rd ed. Oxford: Oxford Univ. Press; 1999</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Chen H, Song YS, Chan PH. Inhibition of NADPH oxidase is neuroprotective after ischemia-reperfusion. J Cereb Blood Flow Metab. 2009;29(7):1262–1272. DOI: 10.1038/jcbfm.2009.47.</mixed-citation><mixed-citation xml:lang="en">Chen H, Song YS, Chan PH. Inhibition of NADPH oxidase is neuroprotective after ischemia-reperfusion. J Cereb Blood Flow Metab. 2009;29(7):1262–1272. DOI: 10.1038/jcbfm.2009.47.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Sies H. Strategies of antioxidant defense. Eur J Biochem. 1993;215(2):213–219. DOI: 10.1111/j.1432-1033.1993.tb18025.x.</mixed-citation><mixed-citation xml:lang="en">Sies H. Strategies of antioxidant defense. Eur J Biochem. 1993;215(2):213–219. DOI: 10.1111/j.1432-1033.1993.tb18025.x.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Kabuto H, Yokoi I, Ogawa N. Melatonin inhibits iron-induced epileptic discharges in rats by suppressing peroxidation. Epilepsia. 1998;39(3):237–243. DOI: 10.1111/j.1528-1157.1998.tb01367.x.</mixed-citation><mixed-citation xml:lang="en">Kabuto H, Yokoi I, Ogawa N. Melatonin inhibits iron-induced epileptic discharges in rats by suppressing peroxidation. Epilepsia. 1998;39(3):237–243. DOI: 10.1111/j.1528-1157.1998.tb01367.x.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Abe K, Nakanishi K, Saito H. The anticonvulsive effect of glutathione in mice. Biol Pharm Bull. 1999;22(11):1177–1179. DOI: 10.1248/bpb.22.1177.</mixed-citation><mixed-citation xml:lang="en">Abe K, Nakanishi K, Saito H. The anticonvulsive effect of glutathione in mice. Biol Pharm Bull. 1999;22(11):1177–1179. DOI: 10.1248/bpb.22.1177.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Rola R, Swiader M, Czuczwar SJ. Electroconvulsions elevate the levels of lipid peroxidation products in mice. Pol J Pharmacol. 2002;54(5): 521–524.</mixed-citation><mixed-citation xml:lang="en">Rola R, Swiader M, Czuczwar SJ. Electroconvulsions elevate the levels of lipid peroxidation products in mice. Pol J Pharmacol. 2002;54(5): 521–524.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Barichello T, Bonatto F, Agostinho FR, et al. Structure-related oxidative damage in rat brain after acute and chronic electroshock. Neurochem Res. 2004;29(9):1749–1753. DOI: 10.1023/b:nere.0000035811.06277.b3.</mixed-citation><mixed-citation xml:lang="en">Barichello T, Bonatto F, Agostinho FR, et al. Structure-related oxidative damage in rat brain after acute and chronic electroshock. Neurochem Res. 2004;29(9):1749–1753. DOI: 10.1023/b:nere.0000035811.06277.b3.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Nieoczym D, Albera E, Kankofer M, et al. Maximal electroshock induces changes in some markers of oxidative stress in mice. J Neural Transm (Vienna). 2008;115(1):19–25. DOI: 10.1007/s00702-007-0805-6.</mixed-citation><mixed-citation xml:lang="en">Nieoczym D, Albera E, Kankofer M, et al. Maximal electroshock induces changes in some markers of oxidative stress in mice. J Neural Transm (Vienna). 2008;115(1):19–25. DOI: 10.1007/s00702-007-0805-6.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Niketiс V, Ristiс S, Saicic ZS, et al. Activities of antioxidant enzymes and formation of the glutathione adduct of hemoglobin (Hb ASSG) in epileptic patients with long-term antiepileptic therapy. Farmaco. 1995;50(11):811–813.</mixed-citation><mixed-citation xml:lang="en">Niketiс V, Ristiс S, Saicic ZS, et al. Activities of antioxidant enzymes and formation of the glutathione adduct of hemoglobin (Hb ASSG) in epileptic patients with long-term antiepileptic therapy. Farmaco. 1995;50(11):811–813.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">El-Shenawy NS, Hamza RZ. Nephrotoxicity of sodium valproate and protective role of L-cysteine in rats at biochemical and histological levels. J Basic Clin Physiol Pharmacol. 2016;27(5):497–504. DOI: 10.1515/jbcpp-2015-0106.</mixed-citation><mixed-citation xml:lang="en">El-Shenawy NS, Hamza RZ. Nephrotoxicity of sodium valproate and protective role of L-cysteine in rats at biochemical and histological levels. J Basic Clin Physiol Pharmacol. 2016;27(5):497–504. DOI: 10.1515/jbcpp-2015-0106.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Arora T, Mehta AK, Sharma KK, et al. Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats. Basic Clin Pharmacol Toxicol. 2009;106(5):372–377. DOI: 10.1111/j.1742-7843.2009.00499.x.</mixed-citation><mixed-citation xml:lang="en">Arora T, Mehta AK, Sharma KK, et al. Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats. Basic Clin Pharmacol Toxicol. 2009;106(5):372–377. DOI: 10.1111/j.1742-7843.2009.00499.x.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
