Abstract
Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. Therefore, antioxidant therapies aimed at reducing oxidative stress have received considerable attention in epilepsy treatment. However, much evidence suggests that oxidative stress does not always have the same pattern in all seizures models. Thus, this review provides an overview aimed at achieving a better understanding of this issue. We summarize work regarding seizure models (i.e.; genetic rat models, kainic acid, pilocarpine, pentylenetetrazol, and trimethyltin), oxidative stress as an etiologic factor in epileptic seizures (i.e.; impairment of antioxidant systems, mitochondrial dysfunction, involvement of redox-active metals, arachidonic acid pathway activation, and aging), and antioxidant strategies for seizure treatment. Combined, this review highlights pharmacological mechanisms associated with oxidative stress in epileptic seizures and the potential for neuroprotection in epilepsy that targets oxidative stress and is supported by effective antioxidant treatment.
Original language | English |
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Pages (from-to) | 122-137 |
Number of pages | 16 |
Journal | Neurochemistry International |
Volume | 59 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2011 Aug |
Bibliographical note
Funding Information:This study was supported by a grant #2011K000271 from the Brain Research Center from 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea . Jae-Hyung Bach was supported by BK 21 program.
Keywords
- Animal models
- Antioxidant strategies
- Epileptic seizures
- Oxidative stress
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Cell Biology