Correlations of oxidative stress markers with niacin sensitivity in male patients with chronic schizophrenia

慢性精神分裂症男性患者氧化应激标志物与烟酸敏感性的相关性

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Abstract

BACKGROUND: Schizophrenia is a debilitating mental disorder linked to oxidative stress (OS) and inflammatory dysregulation. Emerging evidence suggests impaired niacin sensitivity in schizophrenia patients, potentially reflecting OS and inflammation. This study examined the relationships between OS markers and niacin sensitivity in male chronic schizophrenia patients to explore potential pathophysiological mechanisms and identify associated biomarkers. METHODS: The cohort of this cross-sectional study included 80 male chronic schizophrenia patients and 40 matched healthy controls. Blood samples were collected for analysis of nitric oxide (NO), total nitric oxide synthase (TNOS), inducible nitric oxide synthase (iNOS), constitutive nitric oxide synthase (cNOS), total antioxidant capacity (TAC), and vitamin E (VE). Skin niacin sensitivity was assessed via the erythema response to topical niacin. Clinical symptoms were evaluated using the Positive and Negative Syndrome Scale (PANSS). Statistical analyses (t-tests, analysis of variance, and logistic regression) were conducted to identify associations. RESULTS: TNOS, iNOS, cNOS, TAC, and VE levels were significantly lower in the patient group than the healthy control group (p < 0.001). Reduced skin erythema response in patients (p < 0.001) was correlated with lower TAC activity and VE levels. Plasma NO levels were positively correlated with PANSS positive symptom scores (r = 0.370, p = 0.004). TAC was a significant protective predictor of an impaired niacin response (OR = 0.990, p = 0.001). CONCLUSION: Chronic schizophrenia is associated with disrupted redox balance and reduced niacin sensitivity, suggesting an interplay between the oxidative and inflammatory pathways. A weakened niacin response, related to antioxidant deficits, may be linked to the severity of OS. These findings highlight the importance of further research into antioxidant pathways. Additional longitudinal studies are warranted to clarify the nature of these relationships and their clinical relevance.

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