Elevated serum superoxide dismutase and thiobarbituric acid reactive substances in different phases of bipolar disorder and in schizophrenia

There is an increasing body of evidence suggesting that oxidative stress may play a role in the pathophysiology of both schizophrenia (SZ) and bipolar disorder (BD).MethodsWe compared the antioxidant enzyme, serum superoxide dismutase (SOD) and the lipid peroxidation product, thiobarbituric acid reactive substances (TBARS) as assessed in depressed (N = 21), manic (N = 32) and euthymic (N = 31) bipolar patients, and in chronically medicated patients with schizophrenia (N = 97), all fulfilling DSM-IV diagnostic criteria, and a group of healthy controls (N = 32).ResultsSerum SOD (U/mg protein) activity was significantly increased (p < 0.001) in manic (7.44 ± 3.88) and depressed (6.12 ± 4.64) BD patients and SZ (9.48 ± 4.51) when compared to either controls (1.81 ± 0.63) or euthymic (2.75 ± 1.09) BD patients. TBARS (mol/L) levels were significantly higher in the SZ group (4.95 ± 1.56, p = 0.016), bipolar euthymic (6.36 ± 1.46, p < 0.001), bipolar manic (7.54 ± 1.74, p < 0.001), and bipolar depressed patients (5.28 ± 1.54, p = 0.028) compared to controls (3.96 ± 1.51).DiscussionOur findings show increased SOD activity in SZ, as well as in depressed and manic bipolar patients, but not in euthymic BD subjects. This suggests a dysregulation in oxidative defenses in both disorders. It is likely that such changes reflect state changes in bipolar disorder. It is possible that this is a compensatory response to the oxidative stress that occurs in the acute phase of bipolar episodes. TBARS results show increases in lipid peroxidation in mania. TBARS levels in SZ and in euthymic as well as depressed individuals with BD were higher than in controls. This suggests persistent increases in SZ, which may reflect ongoing symptomatology or treatment, and a state dependant gradient in BD, with greatest oxidative stress in mania.These data support oxidative biology as both a key component of the pathophysiology of both BD and SZ, and the use of agents that modulate oxidative biology as a promising avenue for intervention in both disorders.