Barichello Tatiana, Bonatto Fernanda, Feier Gustavo, Martins Marcio R, Moreira Jose Cláudio F, Dal-Pizzol Felipe, Izquierdo Ivan, Quevedo Joao
Laboratorio de Neurotoxicologia, Universidade do Extremo Sul Catarinense, 88806-000 Criciuma, SC, Brazil.
Brain Res. 2004 Jul 16;1014(1-2):177-83. doi: 10.1016/j.brainres.2004.04.026.
Although several advances has occurred over the past 20 years concerning the use of electroconvulsive therapy (ECT), little progress has been made in the mechanisms underlying its therapeutic or adverse effects. Thus, this work was performed in order to determine the level of oxidative damage and antioxidant enzyme activities early and late after acute and chronic electroconvulsive shock (ECS). We demonstrated a decrease in lipid peroxidation in the hippocampus immediately after and up to 30 days after a single or multiple electroconvulsive shock. This was also true for protein carbonyls in the acute protocol. We demonstrated an increase in catalase (CAT) and superoxide dismutase (SOD) activities at different time points after single and multiple electroconvulsive shock. Our findings, for the first time, demonstrated that after electroconvulsive shock, there is an increase in antioxidant enzyme activities and we cannot demonstrate oxidative damage in the hippocampus.
尽管在过去20年里，电休克治疗（ECT）的应用取得了一些进展，但其治疗作用或不良反应的潜在机制却进展甚微。因此，开展这项研究是为了确定急性和慢性电休克（ECS）后早期和晚期的氧化损伤水平及抗氧化酶活性。我们发现，单次或多次电休克后即刻及30天内，海马体中的脂质过氧化作用降低。在急性实验方案中，蛋白质羰基化水平也是如此。我们还发现，单次和多次电休克后的不同时间点，过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性均有所增加。我们的研究结果首次表明，电休克后抗氧化酶活性增加，且未发现海马体存在氧化损伤。
