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Role of oxidative stress in the pathophysiology of schizophrenia

Introduction: The pathophysiology of schizophrenia is still poorly understood. Several studies suggest an important role of inflammation and oxidative stress in this explanation. Schizophrenics seem to have altered defense mechanisms and a distinct response to oxidative stress than that of controls. Oxidative stress is harmful to various cellular structures, among them the extracellular matrix (ECM). A intact and structured ECM is essential for proper synaptic signaling. Objective: To evaluate the response of genes encoding ECM proteins to oxidative stress in chronic schizophrenics and controls. Methodology: Fibroblasts were cultivated from schizophrenic and controls’ skin biopsies. They were treated with TBHQ, a pro-oxidant, or DMSO (the vehicle), and then had the expression of MMP16, GALNT6, SULF1, ADAMTS1 and ACSL1 genes quantified by the method of real time PCR and their products by the method of Western blot. Results: There was response from both groups to oxidative stress, however, this response was different between patients and controls, with schizophrenics expressing less the GALNT6 gene and its protein. Conclusion: GALNT6 gene encodes an enzyme responsible for glycosylating ECM components. We can hypothesize that the schizophrenic’s response to oxidative stress renders the ECM more susceptible to its harmful effects, contributing to the pathophysiology of the disease.