Schizophrenia is a complex neuropsychiatric disorder characterized by a diverse range of symptoms, including positive, negative symptoms such as alogia, anhedonia, avolition, and affective flattening, cognitive symptoms, and emotional symptoms as a separate domain. Emerging evidence suggests that oxidative stress and neuroinflammation play crucial roles in the etiopathogenesis of schizophrenia. The aim of this review is the interplay between oxidative stress—defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses—and neuroinflammatory processes within the central nervous system. Studies indicate that elevated levels of oxidative markers and pro-inflammatory cytokines are commonly observed in individuals with schizophrenia, pointing to a potential pathophysiological link. The dysregulation of redox homeostasis may exacerbate neuroinflammatory responses, contributing to neuronal damage and the subsequent manifestation of psychiatric symptoms. Furthermore, genetic and environmental factors may interact with these biological processes, influencing individual susceptibility to schizophrenia. Understanding the mechanisms by which oxidative stress and neuroinflammation contribute to the development and progression of schizophrenia could pave the way for novel therapeutic strategies aimed at mitigating these pathological processes and improving patient outcomes.