Table 6.
Main findings of ECS/ECT biological mechanisms of action related to the oxidative stress system and mitochondrial bioenergetics.
Kind of Study | Protein/Gene Studied | Population Studied | Main Findings | References |
---|---|---|---|---|
Protein studies | Oxidative stress system mediators | Animal samples | Decrease in oxidative damage parameters in the rat hippocampus. | [137] |
Oxidative stress system mediators | Animal samples | Decrease in lipid peroxidation and protein carbonyls in the rat hippocampus, cerebellum, and striatum after ECS. | [138] | |
Oxidative stress system mediators | Animal samples | Increases in rat hippocampal and cerebellar SOD and GPX activities following ECS. | [139] | |
Oxidative stress system mediators | Animal samples | Decrease in SOD and GPX activity in rats’ brains after ECS. | [140] | |
Oxidative stress system mediators | Animal samples | Delayed oxidative damage after ECS in the rat hippocampus and striatum. | [141] | |
Oxidative stress system mediators | Animal samples | Decrease in mitochondrial respiration and an increase in RNA oxidation in the rat brain tissue after ECS. | [142] | |
Oxidative stress system mediators | Clinical samples | Reduction in serum total oxidant status values and an increase in total antioxidant status in patients with MDD. | [143] | |
Oxidative stress system mediators | Clinical samples | SOD activity decreased after ECT in patients with bipolar disorders and MDD. | [144] |
ECS: electroconvulsive seizure; ECT: electroconvulsive therapy; GPX: glutathione peroxidase; MDD: major depressive disorder; SOD: superoxide dismutase.