A Systematic Review of the Literature Regarding the Relationship Between Oxidative Stress and Electroconvulsive Therapy.

Abstract

Brain's aerobic energy metabolism, abundance of the fatty acids and unsaturated lipids, generation of Reactive Oxygen Species (ROS) by hormones, physiological roles of transition metals (i.e., iron and copper), and free radicals in the nervous system may cause inclination to oxidative stress in psychiatric disorders. Electroconvulsive therapy (ECT) may cause oxidative stress by the electrical field or by the induced seizure. It was aimed to review the literature in terms of the influence of ECT on levels of oxidant and antioxidant compounds. The literature search was performed with the keywords that were oxidative stress or "DNA damage" or "RNA damage" or "lipid peroxidase" or "superoxide dismutase" or "catalase" or "glutathione" or "nitrite" or "nitric oxide" and "electroconvulsive therapy" or "electroconvulsive shock" or "electroconvulsive seizure". Twenty of 1480 records were included. Eleven studies were performed in human subjects, whereas 9 studies were performed in rats. Human studies are conducted with serum, plasma, or urine samples; rat studies include brain tissues from various sites. In rats, four independent studies showed increased levels of lipid oxidation markers, and four independent studies reported increased levels of oxidative stress markers in brain samples. In human studies, studies were performed with circulating blood samples and the results were more inconsistent. Although some markers like superoxide dismutase or thioredoxin imply that ECT may increase the balance for oxidative stress, this notion is not supported by other markers of ECT. The current literature does not clearly suggest that the ECT is associated with oxidative stress in psychiatric disorders. Further studies with similar methods should be performed in big samples.