Lack of association of GPX1 and MnSOD genes with symptom severity and response to clozapine treatment in schizophrenia subjects |
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| Authors: | Renan P Souza Maria Tampakeras Vince Basile Takahiro Shinkai Daniela V F Rosa Steve Potkin Herbert Y Meltzer Jeffrey A Lieberman Marco A Romano‐Silva James L Kennedy |
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| Institution: | 1. Neurogenetics Section, CAMH and Department of Psychiatry, University of Toronto, Toronto, Canada;2. Departamento de Saúde Mental, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil;3. Brain Imaging Center, University of California, Irvine, CA, USA;4. Departments of Psychiatry and Pharmacology, Vanderbilt University, Nashville, TN, USA;5. Department of Psychiatry, University of North Carolina, Chapel Hill, NC, USA |
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| Abstract: | Abnormal activities of critical antioxidant enzymes and other indices of lipid peroxidation in plasma and red blood cells were detected in patients with schizophrenia. Other results have shown that oxidative stress may be modulated by clozapine. Based on that and some studies already found different clinical relations between reactive oxygen species and negative and positive symptoms, we evaluated association between clinical response and the polymorphism in the human glutathione peroxidase (GPX1) (Pro200Leu, rs1050450) and manganese SOD (MNSOD) (Ala16Val, rs4880) gene in 216 clozapine‐treated patients with schizophrenia. No association was found with these two functional polymorphisms and clozapine response and symptom change after 6 months. No correlations were found between positive/negative symptoms score and both polymorphisms. Our results present that GPX1 (Pro200Leu) and MNSOD (Ala16Val) polymorphisms seem do not play a central role in the clozapine response, although studies in larger and independent samples are necessary to confirm our findings. Copyright © 2009 John Wiley & Sons, Ltd. |
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| Keywords: | MnSOD GPX1 schizophrenia clozapine BPRS gene– gene interaction |
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