Year: 2026 | Month: April-June | Volume: 11 | Issue: 2 | Pages: 1-8
DOI: https://doi.org/10.52403/ijshr.20260201
Disrupted Oxidative-Antioxidant Balance in Schizophrenia: A Case-Control Study Evaluating Serum Malondialdehyde and Plasma Superoxide Dismutase
Arpan Kumar Ghosh1, Niloy Kumar Das2, Kalyan Kumar Bhowmik3, Arunima Chaudhuri4
1Associate Professor, Department of Physiology, College of Medicine & JNM Hospital, WBUHS, Kalyani, Nadia, West Bengal, India.
2Assistant Professor, Department of Anatomy, College of Medicine & JNM Hospital, WBUHS, Kalyani, Nadia, West Bengal, India.
3Assistant Professor, Department of General Medicine, JMN Medical College, Chakdaha, Nadia, West Bengal, India.
4Professor and Head, Department of Physiology, Burdwan Medical College, Purba Bardhaman, West Bengal, India.
Corresponding Author: Dr. Arpan Kumar Ghosh
ABSTRACT
Background: Schizophrenia is a chronic neuropsychiatric disorder in which oxidative stress has been implicated as a key pathogenic mechanism. Imbalance between free radical generation and antioxidant defense may contribute to neuronal damage. This study aimed to evaluate oxidative stress and antioxidant status in schizophrenia by estimating serum malondialdehyde (MDA) and plasma superoxide dismutase (SOD) respectively, and to examine their interrelationship.
Methods: This analytical case–control study included 50 participants aged 18–40 years, comprising 25 patients with schizophrenia (diagnosed according to ICD-10 criteria) and 25 age- and sex-matched healthy controls. Serum MDA levels were estimated using the thiobarbituric acid reactive substances method, while plasma SOD activity was measured spectrophotometrically using the PMS–NBT method. Data were analyzed using independent samples Student’s t-test and Pearson’s correlation. A p-value <0.05 was considered statistically significant.
Results: Mean serum MDA levels were significantly higher in cases compared to controls (5.61 ± 0.36 vs 2.84 ± 0.61 nmol/mL; p < 0.001). Plasma SOD activity did not differ significantly between cases and controls (9.40 ± 1.62 vs 9.04 ± 1.87 U/mL; p = 0.470). Pearson’s correlation analysis revealed no significant association between MDA and SOD in cases (r = 0.058, p = 0.784), whereas a moderate positive correlation was observed in controls (r = 0.597, p = 0.002).
Conclusion: The findings indicate increased lipid peroxidation in schizophrenia, reflecting enhanced oxidative stress, without a proportional antioxidant response. The absence of correlation between MDA and SOD in patients suggests disrupted oxidative–antioxidant balance. These results support the role of oxidative stress in the pathophysiology of schizophrenia and highlight the potential relevance of redox biomarkers in future research.
Keywords: Schizophrenia; Oxidative Stress; Malondialdehyde; Superoxide Dismutase; Lipid Peroxidation; Antioxidants