en O 22: Reactive Oxygen Species and Epilepsy تحقیقات پایه در علوم اعصاب Basic research in Neuroscience مروری Review --- Open Access, CC-BY-NC <table border="0" cellpadding="5px" cellspacing="2" dir="rtl" id="table_article" style="font-family: Tahoma; background-color: rgb(251, 250, 249); break-inside: avoid !important;" width="100%"> <tbody style="break-inside: avoid !important; font-size: 12px; margin-top: 0px; line-height: 2.2; margin-bottom: 0px; text-align: justify;"> <tr style="break-inside: avoid !important;"> <td class="abstractmed" colspan="2" style="break-inside: avoid !important;"> <p style="margin-top: 0px; margin-bottom: 0px; text-align: center;"><span style="color: rgb(0, 0, 0); line-height: 20.8px;">لطفاً به چکیده انگلیسی مراجعه شود.</span></p> </td> </tr> <tr style="break-inside: avoid !important;"> </tr> </tbody> </table> <p></p> <p>Seizure activity has been proposed to result in the generation of reactive oxygen species (ROS), which then contribute to seizure-induced neuronal damage and eventually cell death. Although the mechanisms of seizure-induced ROS generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. We aim to determine the sources of seizure-induced ROS and their contribution to seizure-induced cell death. Live cell imaging techniques in glio-neuronal cultures and in ex vivo epileptic brain tissue. We show that prolonged seizure-like activity increases ROS production in an NMDA receptor-dependent manner. Unexpectedly, however, mitochondria did not contribute to ROS production during seizure-like activity. ROS were generated primarily by NADPH oxidase and later by xanthine oxidase (XO) activity in a calcium-independent manner. Inhibition of NADPH or XO markedly reduced seizure-like activity-induced neuronal apoptosis. In addition, ROS were upregulated in chronic epilepsy in ex vivo brain slices. Inhibition of ROS production in vivo by AEBSF, a NADPH oxidase inhibitor, markedly reduced seizure-induced cell death. These findings demonstrate a critical role for ROS, generated by NADPH oxidase, contributing to seizure-induced cell death. These findings point to NADPH oxidase inhibition as a novel treatment strategy to prevent brain injury in seizures, status epilepticus and chronic epilepsy.&nbsp;</p> Cell Death, Epilepsy, Brain Injury 22 22 http://shefayekhatam.ir/browse.php?a_code=A-10-24-839&slc_lang=en&sid=1 S Kovac S Kovac stjepana.kovac@ukmuenster.de 100319475328460011752 100319475328460011752 Yes University Hospital Münster, Münster, Germany University Hospital Münster, Münster, Germany S Williams S Williams 100319475328460011753 100319475328460011753 No University College London, London, UK University College London, London, UK AM Domijan AM Domijan 100319475328460011754 100319475328460011754 No University College London, London, UK University College London, London, UK MC Walker MC Walker 100319475328460011755 100319475328460011755 No University College London, London, UK University College London, London, UK AY Abramov AY Abramov 100319475328460011756 100319475328460011756 No University College London, London, UK University College London, London, UK