Role of Oxidative Stress in Pathophysiological Progression of Schizophrenia

Abstract

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