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About the Authors:
Jeffrey K. Yao
* E-mail: [email protected]
Affiliations VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States of America, Department of Psychiatry, University of Pittsburgh Medical Center, Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States of America, Department of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, Pennsylvania, United States of America
George G. Dougherty Jr.
Affiliations VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States of America, Department of Psychiatry, University of Pittsburgh Medical Center, Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States of America
Ravinder D. Reddy
Affiliations VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, United States of America, Department of Psychiatry, University of Pittsburgh Medical Center, Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States of America
Matcheri S. Keshavan
Affiliations Department of Psychiatry, University of Pittsburgh Medical Center, Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States of America, Beth Israel Deaconess Medical Center and Harvard University, Boston, Massachusetts, United States of America
Debra M. Montrose
Affiliation: Department of Psychiatry, University of Pittsburgh Medical Center, Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States of America
Wayne R. Matson
Affiliation: Bedford VA Medical Center, Bedford, Massachusetts, United States of America
Joseph McEvoy
Affiliation: Duke University Medical Center, Durham, North Carolina, United States of America
Rima Kaddurah-Daouk
Affiliation: Duke University Medical Center, Durham, North Carolina, United States of America
Introduction
Schizophrenia (SZ) is a highly disabling disease characterized by widespread structural and functional brain alterations, the pathogenesis of which remains poorly understood. It has been proposed that at least in part, the neuropathological changes in this illness may result from oxidative stress mechanisms [1]–[10]. The precise components of such alterations remain unclear.
Biological systems have evolved complex protective strategies against free radical toxicity. Under physiological conditions the potential for free radical-mediated damage is kept in check by the antioxidant defense system (AODS), comprising a series of enzymatic and non-enzymatic components. These enzymes act cooperatively at different sites in the free radical pathways. Recently, we have observed that a dynamic state is kept in check during the redox coupling under normal conditions [11]. By contrast, lack of such correlations in brains of SZ patients point to a disturbance of redox coupling mechanisms in the AODS, possibly resulting from a decreased level...