Nieoczym D, Albera E, Kankofer M, Wlaź P
Department of Animal Physiology, Institute of Biology, Maria Curie-Skłodowska University, Lublin, Poland.
J Neural Transm (Vienna). 2008;115(1):19-25. doi: 10.1007/s00702-007-0805-6. Epub 2007 Aug 31.
The oxidative/antioxidative status was investigated in maximal electroshock-induced seizures in mice, a well established model of generalized seizures in humans. Mice were given a single electroshock resulting in tonic convulsions. Total antioxidant capacity (TAC), lipid peroxidation intensity and glutathione peroxidase (GSH-Px) activity was measured spectrophotometrically in the brain, plasma and erythrocytes collected from mice sacrificed at different time points after stimulation. For comparison, sham-stimulated and subeffectively stimulated (no tonic seizures) mice were used. Tonic seizures caused an immediate increase in GSH-Px activity in the brain and during the following three hours the enzyme activity decreased below control values. Similar changes were seen after subconvulsive stimulations, however, a significant increase occurred only one hour after electroshock. A marked TAC reduction in the brain was observed three hours after subconvulsive stimulations. Nevertheless, no significant changes in TAC after tonic seizures were noted. TAC in plasma was significantly reduced three hours after both subconvulsive and convulsive stimulation. Marked reduction of lipid peroxidation intensity in the brain and plasma was recorded after both modes of stimulation. In conclusion, pronounced changes in oxidative/antioxidative status in mice following electroshock are caused by both convulsive and subconvulsive stimuli. Participation of oxidative stress in seizures and pathophysiology of epilepsy awaits further clarification.
在小鼠最大电休克诱导的癫痫发作中研究了氧化/抗氧化状态,这是一种已确立的人类全身性癫痫发作模型。给小鼠单次电休克,导致强直性惊厥。在刺激后不同时间点处死小鼠,分光光度法测定其大脑、血浆和红细胞中的总抗氧化能力(TAC)、脂质过氧化强度和谷胱甘肽过氧化物酶(GSH-Px)活性。作为对照,使用假刺激和亚有效刺激(无强直性癫痫发作)的小鼠。强直性癫痫发作导致大脑中GSH-Px活性立即增加,在接下来的三个小时内,该酶活性降至对照值以下。亚惊厥刺激后也观察到类似变化,然而,仅在电休克后一小时出现显著增加。亚惊厥刺激三小时后观察到大脑中TAC明显降低。然而,强直性癫痫发作后TAC未观察到显著变化。亚惊厥和惊厥刺激三小时后血浆中TAC均显著降低。两种刺激方式后均记录到大脑和血浆中脂质过氧化强度明显降低。总之,电休克后小鼠氧化/抗氧化状态的明显变化是由惊厥和亚惊厥刺激引起的。氧化应激在癫痫发作和癫痫病理生理学中的作用有待进一步阐明。