Dysfunctional oxidative stress response in first-episode of schizophrenia

Abstract

Purpose: To investigate the probable effect of oxidative stress on cognitive deficits in schizophrenia. Methods: A total of 149 first-episode schizophrenia (FES) patients and 65 healthy controls were enrolled in this study. Psychiatric symptoms were evaluated using Positive and Negative Syndrome Scale, while cognitive function was assessed using MATRICS Consensus Cognitive Battery. Oxidative parameters, including glutathione (GSH), thioredoxin (TRX), nitric oxide (NO), homocysteine (Hcy) and superoxide dismutase (SOD)]; hypersensitive C-reactive protein (Hs-CRP, an inflammation marker); lipopolysaccharide (LPS) and CD4+T cell sub-sets (Th1, Th2, Th17 and Treg cells) were measured in all subjects, while PANSS was evaluated in FES patients only. Results: Levels of the oxidants, NO, Hcy and inflammatory parameters (Hs-CRP, LPS, Th1, Th2 and Th17) were higher in FES patients than in controls (p < 0.05). In contrast, levels of antioxidants (GSH and SOD) in FES patents were lower than those in controls (p < 0.05). Moreover, TRX was higher in schizophrenia patients than in controls (p < 0.05). The changes in levels of these biomarker indicated oxidative stress responses. There were statistically significant differences in hemogram and T cell subtype between FES and control (p < 0.05). Results from fMRI analysis revealed schizophrenia- induced lesions in the encephalic region associated with cognition function. Conclusion: Oxidative stress (OS) induces immune response which eventually leads to impairment of cognition.