The evidence about the role of oxidative stress on the pathophysiology of bipolar disorder (BD) has been increased recently. It has been considered that oxidative stress and its effects cause damage in the critical brain circuits regulating affective functions, emotions, motor behaviors and so that the symptoms seen in BD occur by the deterioration of mood-stabilizing mechanisms. In clinical trials, significant changes were determined in the BD patients levels of antioxidant enzymes, lipid peroxidation and nitric oxide. Because of the different clinical features of the disorder such as manic/hypomanic, depressive, or mixed episode, the data associated with oxidative stress might vary among the patients. Some mood stabilizers used in the treatment are known to have antioxidant effects. Normalization of the oxidative stress parameters had been reported in the treatment process of BD. It makes a positive contribution to the treatment process that these drugs increase the neurotrophic factors and protect against apoptosis as well as reducing the effects of oxidative stress. Reactive oxygen species occur with the escape of some electrons from the chain during their flow in the mitochondria complex and mitochondrial dysfunction develops after the inhibition of electron transport chain. Mitochondrial dysfunction found to be associated with the pathogenesis of BD. Mitochondrial dysfunction and oxidative stress may create symptoms of the BD secondary to the changes in intracellular signaling system, balance of intracellular calcium, and DNA structure. Using antioxidants, in addition to the treatment, is expected to provide positive contribution to the prognosis in bipolar patients. Systematic studies including each period of the disorder are needed for using the findings indicating deterioration of oxidative balance as biological markers in BD.
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