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Lack of association of GPX1 and MnSOD genes with symptom severity and response to clozapine treatment in schizophrenia subjects
Author(s) -
Souza Renan P.,
Tampakeras Maria,
Basile Vince,
Shinkai Takahiro,
Rosa Daniela V. F.,
Potkin Steve,
Meltzer Herbert Y.,
Lieberman Jeffrey A.,
RomanoSilva Marco A.,
Kennedy James L.
Publication year - 2009
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.1076
Subject(s) - clozapine , gpx1 , medicine , oxidative stress , schizophrenia (object oriented programming) , glutathione peroxidase , antioxidant , lipid peroxidation , endocrinology , psychiatry , superoxide dismutase , biology , biochemistry
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.