TY  - JOUR
TI  - Reactive oxygen species in status epilepticus
KW  - Mitochondria
KW  -  NADPH oxidase
KW  -  Nrf2
KW  -  Oxidative stress
KW  -  Reactive oxygen species
KW  -  Status epilepticus
UR  - https://doi.org/10.1016/j.yebeh.2019.07.011
JF  - Epilepsy & Behavior
AV  - public
ID  - discovery10085309
SN  - 1525-5069
N1  - This version is the author accepted manuscript. For information on re-use, please refer to the publisher?s terms and conditions.
VL  - 101
A1  - Shekh-Ahmad, T
A1  - Kovac, S
A1  - Abramov, AY
A1  - Walker, MC
Y1  - 2019/12//
IS  - B
N2  - There has been growing evidence for a critical role of oxidative stress in neurodegenerative disease, providing novel targets for disease modifying treatments. Although antioxidants have been suggested and tried in the treatment of epilepsy, it is only recently that the pivotal role of oxidative stress in the pathophysiology of status epilepticus has been recognized. Although conventionally thought to be generated by mitochondria, reactive oxygen species during status epilepticus and prolonged seizure are generated mainly by NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (stimulated by NMDA receptor activation). Excessive production of reactive oxygen species results in lipid peroxidation, DNA damage, enzyme inhibition, and mitochondrial damage, culminating in neuronal death. Antioxidant therapy has been hampered by poor CNS penetration and rapid consumption by oxidants. However, alternative approaches such as inhibiting NADPH oxidase or increasing endogenous antioxidant defenses through activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) could avoid these problems. Small molecules that increase Nrf2 activation have proven to be not only effective neuroprotectants following status epilepticus, but also potently antiepileptogenic. There are "Proceedings of the 7th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures".
ER  -