Walker, Matthew C;
(2023)
Reactive oxygen species in Status Epilepticus.
Epilepsia Open
10.1002/epi4.12691.
(In press).
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Abstract
It has long been recognized that status epilepticus can cause considerable neuronal damage, and this has become one of its defining features. The mechanisms underlying this damage are less clear. Excessive activation of NMDA receptors results in large rises in internal calcium, which eventually lead to neuronal death. Between NMDA receptor activation and neuronal death are a number of intermediary steps, key amongst which is the generation of free radicals, and reactive oxygen and nitrogen species. Although it has long been thought that mitochondria are the primary source for reactive oxygen species, more recent evidence has pointed to a prominent role for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, an enzyme localized in cell membranes. There is burgeoning in vivo and in vitro evidence that therapies that target the production or removal of reactive oxygen species are not only effective neuroprotectants following status epilepticus, but also potently antiepileptogenic. Moreover, combining therapies targeted at inhibiting NADPH oxidase and at increasing endogenous antioxidants seem to offer the greatest benefits.
Type: | Article |
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Title: | Reactive oxygen species in Status Epilepticus |
Location: | United States |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.1002/epi4.12691 |
Publisher version: | https://doi.org/10.1002/epi4.12691 |
Language: | English |
Additional information: | © 2023 The Author. Epilepsia Open published by Wiley Periodicals LLC on behalf of International League Against Epilepsy. This is an open access article under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/). |
Keywords: | excitotoxicity, free radicals, mitochondria, reactive oxygen species, status epilepticus |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Experimental Epilepsy |
URI: | https://discovery.ucl.ac.uk/id/eprint/10164079 |
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