Búrigo Márcio, Roza Clarissa A, Bassani Cintia, Fagundes Diego A, Rezin Gislaine T, Feier Gustavo, Dal-Pizzol Felipe, Quevedo João, Streck Emilio L
Laboratório de Bioquímica Experimental, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil,
Neurochem Res. 2006 Nov;31(11):1375-9. doi: 10.1007/s11064-006-9185-9. Epub 2006 Oct 25.
It is well described that impairment of energy production has been implicated in the pathogenesis of a number of diseases. Although several advances have occurred over the past 20 years concerning the use and administration of electroconvulsive therapy (ECT) to minimize its side effects, little progress has been made in understanding its mechanism of action. In this work, our aim was to measure the activities of mitochondrial respiratory chain complexes II and IV and succinate dehydrogenase from rat brain after acute and chronic electroconvulsive shock (ECS). Our results showed that mitochondrial respiratory chain enzymes activities were increased after acute ECS in hippocampus, striatum and cortex of rats. Besides, we also demonstrated that complex II activity was increased after chronic ECS in cortex, while hippocampus and striatum were not affected. Succinate dehydrogenase, however, was inhibited after chronic ECS in striatum, activated in cortex and not affected in hippocampus. Finally, complex IV was not affected by chronic ECS in hippocampus, striatum and cortex. Our findings demonstrated that brain metabolism is altered by ECS.
能量产生受损与多种疾病的发病机制有关，这一点已有充分描述。尽管在过去20年里，关于使用和管理电惊厥治疗（ECT）以尽量减少其副作用方面已经取得了一些进展，但在理解其作用机制方面进展甚微。在这项工作中，我们的目的是测量急性和慢性电惊厥休克（ECS）后大鼠脑中线粒体呼吸链复合物II和IV以及琥珀酸脱氢酶的活性。我们的结果表明，急性ECS后，大鼠海马、纹状体和皮质中的线粒体呼吸链酶活性增加。此外，我们还证明，慢性ECS后皮质中的复合物II活性增加，而海马和纹状体未受影响。然而，慢性ECS后纹状体中的琥珀酸脱氢酶受到抑制，皮质中被激活，海马中未受影响。最后，慢性ECS对海马、纹状体和皮质中的复合物IV没有影响。我们的研究结果表明，ECS会改变脑代谢。
