No evidence for oxidative damage in the hippocampus after acute and chronic electroshock in rats.
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.
Barichello
Tatiana
T
Laboratorio de Neurotoxicologia, Universidade do Extremo Sul Catarinense, 88806-000 Criciuma, SC, Brazil.
Bonatto
Fernanda
F
Feier
Gustavo
G
Martins
Marcio R
MR
Moreira
Jose Cláudio F
JC
Dal-Pizzol
Felipe
F
Izquierdo
Ivan
I
Quevedo
Joao
J
D000222:Adaptation, Physiological; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004597:Electroshock / Q000009:adverse effects*; D006624:Hippocampus / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D002374:Catalase; D013482:Superoxide Dismutase