Role of Oxidative Stress in Pathophysiological Progression of Schizophrenia

Abstract

Background: Oxidative stress (OS) is a chief contributing factor to the pathological advancement of Schizophrenia (SCZ). In recent years, OS has emerged as an important aspect in SCZ research and provides abundant opportunities and expectations for a better understanding of its pathophysiology, which may lead to novel treatment strategies. Introduction: The increased OS and formation of reactive oxygen species (ROS) leads to damage to cellular macromolecules. The excessive OS is associated with several physiological processes, such as dysfunction of mitochondria and neuroglia, inflammation, underactive Nmethyl- D-aspartate (NMDA) receptors, and the abnormalities of fast-spiking gammaaminobutyric acid (GABA) interneurons. Methods: The methods adopted for the study are mainly based on the secondary search through a systemic literature review. The role of various anti-oxidants, including vitamins, is discussed in the reduction of SCZ. Results: Various preclinical and clinical studies suggest the involvement of OS and ROS in the progression of the disease. Recent human trials have shown the treatment with antioxidants to be effective in ameliorating symptoms and delaying the progression of SCZ pathology. The studies have demonstrated that innate and dietary antioxidants exert beneficial effects by reducing the severity of positive symptoms (PS) and/or negative symptoms (NS) of SCZ. Conclusion: The present review critically evaluates the effect of antioxidants and highlights the role of OS in SCZ.