Lores Arnaiz S, Travacio M, Llesuy S, Rodríguez de Lores Arnaiz G
Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Neurochem Res. 1998 Dec;23(12):1477-83. doi: 10.1007/BF03177490.
We evaluated oxidative stress associated with a model of experimental epilepsy. Male Wistar rats were injected i.p. with 150 mg/kg convulsant 3-mercaptopropionic acid and decapitated in two stages: during seizures or in the post-seizure period. Spontaneous chemiluminescence, levels of thiobarbituric acid reactive substances, total antioxidant capacity and antioxidant enzyme activities were measured in cerebellum, hippocampus, cerebral cortex and striatum. In animals killed at seizure, increases of 42% and 90% were observed in spontaneous chemiluminescence of cerebellum and cerebral cortex homogenates, respectively, accompanied by a 25% increase in cerebral cortex levels of thiobarbituric acid reactive substances. In the post-seizure stage, emission completely returned to control levels in cerebral cortex and partly in cerebellum, thus showing oxidative stress reversibility in time. Hippocampus and striatum seemed less vulnerable areas to oxidative damage. A 30% decrease in glutathione peroxidase activity was only observed in cerebral cortex during seizures, while catalase and superoxide dismutase remained unchanged in all four areas during either stage. Likewise, total antioxidant capacity was unaffected in any of the studied areas. It is suggested that oxidative stress in this model of epilepsy arises from an increase in oxidant species rather than from depletion of antioxidant defences.
我们评估了与实验性癫痫模型相关的氧化应激。雄性Wistar大鼠腹腔注射150mg/kg惊厥剂3-巯基丙酸，并分两个阶段断头：在癫痫发作期间或癫痫发作后阶段。测量了小脑、海马、大脑皮层和纹状体中的自发化学发光、硫代巴比妥酸反应性物质水平、总抗氧化能力和抗氧化酶活性。在癫痫发作时处死的动物中，小脑和大脑皮层匀浆的自发化学发光分别增加了42%和90%，同时大脑皮层硫代巴比妥酸反应性物质水平增加了25%。在癫痫发作后阶段，大脑皮层的发光完全恢复到对照水平，小脑部分恢复，从而显示出氧化应激在时间上的可逆性。海马和纹状体似乎是氧化损伤较不易发生的区域。仅在癫痫发作期间大脑皮层中观察到谷胱甘肽过氧化物酶活性降低30%，而在两个阶段中，过氧化氢酶和超氧化物歧化酶在所有四个区域均保持不变。同样，在所研究的任何区域中总抗氧化能力均未受影响。提示该癫痫模型中的氧化应激源于氧化剂种类的增加而非抗氧化防御的耗竭。
