| Literature DB >> 21672578 |
Eun-Joo Shin1, Ji Hoon Jeong, Yoon Hee Chung, Won-Ki Kim, Kwang-Ho Ko, Jae-Hyung Bach, Jau-Shyong Hong, Yukio Yoneda, Hyoung-Chun Kim.
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.Entities:
Mesh:
Year: 2011 PMID: 21672578 PMCID: PMC3606551 DOI: 10.1016/j.neuint.2011.03.025
Source DB: PubMed Journal: Neurochem Int ISSN: 0197-0186 Impact factor: 3.921