Role of oxidative stress in epileptic seizures

被引：343

作者：

Shin, Eun-Joo ^{[1
]}

Jeong, Ji Hoon ^{[2
]}

Chung, Yoon Hee ^{[3
]}

Kim, Won-Ki ^{[4
]}

Ko, Kwang-Ho ^{[5
]}

Bach, Jae-Hyung ^{[1
]}

Hong, Jau-Shyong ^{[6
]}

Yoneda, Yukio ^{[7
]}

Kim, Hyoung-Chun ^{[1
]}

机构：

[1] Kangwon Natl Univ, Coll Pharm, Neuropsychopharmacol & Toxicol Program, Chunchon 200701, South Korea

[2] Chung Ang Univ, Dept Pharmacol, Coll Med, Seoul 156756, South Korea

[3] Chung Ang Univ, Dept Anat, Coll Med, Seoul 156756, South Korea

[4] Korea Univ, Dept Neurosci, Coll Med, Seoul 136705, South Korea

[5] Cha Univ, Coll Pharm, Pochon 487801, South Korea

[6] NIEHS, Neuropharmacol Sect, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA

[7] Kanazawa Univ, Mol Pharmacol Lab, Div Pharmaceut Sci, Grad Sch Nat Sci & Technol, Kanazawa, Ishikawa 9201192, Japan

来源：

NEUROCHEMISTRY INTERNATIONAL | 2011年 / 59卷 / 02期

关键词：

Epileptic seizures; Oxidative stress; Antioxidant strategies; Animal models; PILOCARPINE-INDUCED SEIZURES; PENTYLENETETRAZOL-INDUCED SEIZURES; KAINATE-INDUCED NEUROTOXICITY; PLACEBO-CONTROLLED TRIAL; GLUTATHIONE-S-TRANSFERASE; TEMPORAL-LOBE EPILEPSY; ACID-INDUCED SEIZURES; THIOL REDOX STATE; ADD-ON THERAPY; SENESCENCE-ACCELERATED MOUSE;

D O I：

10.1016/j.neuint.2011.03.025

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：122 / 137

页数：16

共 245 条

[1]

ALI SF, 1992, NEUROTOXICOLOGY, V13, P637

[2] Enhanced calcium influx in hippocampal CA3 neurons of spontaneously epileptic rats [J].