It is important, therefore, to understand and identify the key mechanisms involved from the insult to epilepsy to provide prophylactic treatment for preventing epilepsy development in those at risk. Many of the epilepsies are acquired conditions following an insult to the brain such as a prolonged seizure, traumatic brain injury (TBI), or stroke. Despite substantial progress in epilepsy research, approximately 35% of all epilepsy patients are resistant to anti-seizure drugs (ASDs) and continue to experience recurrent unprovoked spontaneous seizures. This review also discusses reliable methods for the assessment of ROS, OS markers, and their by-products in epilepsy clinical studies.Įpilepsy remains one of the most common neurological diseases, affecting over 70 million people worldwide, which imposes enormous physical, psychological, social, and economic burdens on patients, their caregivers, and society. The indirect detection of secondary products of ROS such as measurements of DNA damage, lipid peroxidation, and protein oxidation will also be discussed. In addition, we discuss the role of these ROS and markers of oxidative injury in acute seizures and epilepsy pre-clinical studies. We then discuss general methods and assays used for the ROS measurements, mainly superoxide anion, hydrogen peroxide, peroxynitrite, and hydroxyl radical in in vitro and in vivo studies. We first provide pieces of evidence for the involvement of different sources of ROS in epilepsy. In this manuscript, we review the current reliable methods for quantifying ROS-related and OS-related markers in pre-clinical and clinical epilepsy studies. Seizure-induced damage has been demonstrated both in vitro and in several in vivo seizure and epilepsy models by direct determination of ROS, and by measuring indirect markers of OS. Oxidative stress (OS) and excessive reactive oxygen species (ROS) production have been implicated in many neurological pathologies, including acute seizures and epilepsy.
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