Ueda Yuto, Nakajima Akira, Tokumaru Jun
Department of Psychiatry, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki, Japan.
Neurochem Res. 2003 Dec;28(12):1895-900. doi: 10.1023/a:1026136211759.
To analyze antioxidant ability and lipid peroxidation in the hippocampus of rats in an interictal state of FeCl3-induced epileptogenesis, the hippocampal eliminating decay ratio of exogenously applied nitroxide radical (3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (carbamoyl-PROXYL)) by electron paramagnetic resonance (EPR) spectroscopy, and the thiobarbituric reactive substances (TBARS) level in the hippocampus were measured. The prolonged half-life of electron paramagnetism of carbamoyl-PROXYL in the hippocampus of rats with chronic FeCl3-induced epileptogenesis revealed decreased antioxidant ability, which supports the vulnerability against oxidative stress. In addition, TBARS level (marker of lipid peroxidation) was increased in the hippocampus of rats injected with FeCl3 compared with that of control. This study revealed that repetitive seizures resulted in the decreased hippocampal antioxidant ability with lipid peroxidation and explained the regional vulnerability to oxidative stress in the limbic system with epileptogenesis.
为分析氯化铁诱导癫痫发作形成的发作间期大鼠海马体中的抗氧化能力和脂质过氧化情况，通过电子顺磁共振（EPR）光谱法测定了海马体对外源性应用的氮氧自由基（3-氨基甲酰基-2,2,5,5-四甲基吡咯烷-1-氧基（氨基甲酰基- PROXYL））的消除衰减率，并测量了海马体中的硫代巴比妥酸反应性物质（TBARS）水平。在慢性氯化铁诱导癫痫发作形成的大鼠海马体中，氨基甲酰基- PROXYL的电子顺磁性半衰期延长，表明抗氧化能力下降，这支持了对氧化应激的易感性。此外，与对照组相比，注射氯化铁的大鼠海马体中TBARS水平（脂质过氧化的标志物）升高。本研究表明，反复癫痫发作导致海马体抗氧化能力下降并伴有脂质过氧化，解释了癫痫发作形成时边缘系统对氧化应激的区域易感性。
