No evidence for oxidative damage in the hippocampus after acute and chronic electroshock in rats

Brain Res. 2004 Jul 16;1014(1-2):177-83. doi: 10.1016/j.brainres.2004.04.026.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Antioxidants / metabolism
  • Catalase / metabolism
  • Electroshock / adverse effects*
  • Hippocampus / metabolism*
  • Lipid Peroxidation
  • Male
  • Oxidative Stress*
  • Rats
  • Rats, Wistar
  • Superoxide Dismutase / metabolism

Substances

  • Antioxidants
  • Catalase
  • Superoxide Dismutase