Aims: There is evidence that dysregulation of free radicals metabolism associated with abnormal activities of antioxidative enzymes in schizophrenia can lead to lipid peroxidation in plasma, erythrocytes, blood platelets and cerebrospinal fluid. Injury to neurons in schizophrenia may affect their function, i.e. membrane transport, impairment of energy production in mitochondria, changes in membrane phospholipid composition, alteration of receptors and transporters as well as neurotransmission. The purpose of the present study was to assess the total antioxidant capacity (TAC) and lipid peroxidation (expressed as the level of thiobarbituric acid reactive substances [TBARS]) in plasma from schizophrenic patients taking olanzapine or risperidone. The level of TBARS estimated according to the Rice-Evans method and TAC ([ABTS; 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radical cation decolorization assay]) in plasma from schizophrenic patients (DSM-IV criteria for schizophrenia, n = 30, age 18-36) taking olanzapine or risperidone and from healthy volunteers (n = 30) were measured.
Methods: The level of TBARS in plasma from healthy volunteers after incubation with olanzapine or risperidone was also estimated.
Results: Significantly lower plasma TAC (P < 0.05) and significantly increased level of TBARS (P < 0.001) in schizophrenic patients were observed. The in vitro study showed that after olanzapine or risperidone (at final concentrations corresponding to doses used in acute episodes of schizophrenia treatment) no changes of plasma lipid peroxidation were found (P > 0.05). The obtained results indicate that the pro-oxidant disturbances occur in schizophrenic patients (acute episode) taking stable doses of olanzapine or risperidone.
Conclusion: It seems that second-generation antipsychotics (olanzapine and risperidone) are not responsible for increase of plasma lipid peroxidation.
© 2010 The Authors. Psychiatry and Clinical Neurosciences © 2010 Japanese Society of Psychiatry and Neurology.