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Oxidative stress in tardive dyskinesia: genetic association study and meta-analysis of NADPH quinine oxidoreductase 1 (NQO1) and Superoxide dismutase 2 (SOD2, MnSOD) genes.
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Feb 01; 34(1):50-6.PN

Abstract

INTRODUCTION

Tardive dyskinesia (TD) is a potentially irreversible side effect of antipsychotic medication treatment that occurs in approximately 25% of chronically treated schizophrenia patients. Oxidative stress has been one of the proposed mechanisms influencing TD risk. Pae et al. (2004) originally reported a significant association between TD and the NADPH quinine oxidoreductase 1 (NQO1) gene Pro187Ser (C609T, rs1800566) polymorphism in Korean schizophrenia patients; however, subsequent studies have not consistently replicated these findings. Similarly, Hori et al. (2000) reported an association between TD and the Manganese superoxide dismutase SOD2 (MnSOD) gene Ala9Val (rs4880) polymorphism in a Japanese sample, but most research groups failed to replicate their positive findings.

AIMS

We investigated the role of the NQO1 polymorphism Pro187Ser and SOD2 (Ala9Val) in a group of well-characterized schizophrenia patients (N=223) assessed for TD. We also performed a meta-analysis of all the previously published TD studies, including data from our sample, on these polymorphisms, Pro187Ser (N=5 studies) and Ala9Val (N=9 studies).

RESULTS

We did not observe a significant association of the Pro187Ser or Ala9Val polymorphism with TD occurrence or AIMS scores in our Caucasian and African American samples when analyzed independently. Meta-analysis did not reveal a significant association of the Pro187Ser/Ala9Val alleles or genotypes with TD occurrence.

CONCLUSIONS

Neither the NQO1 Pro187Ser nor the SOD2 Ala9Val appear to play a major role in TD risk, although additional polymorphisms should be tested before the role of NQO1 and SOD2 in TD can be completely excluded.

Authors+Show Affiliations

Neurogenetics Section, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario, Canada M5T 1R8.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19778569

Citation

Zai, Clement C., et al. "Oxidative Stress in Tardive Dyskinesia: Genetic Association Study and Meta-analysis of NADPH Quinine Oxidoreductase 1 (NQO1) and Superoxide Dismutase 2 (SOD2, MnSOD) Genes." Progress in Neuro-psychopharmacology & Biological Psychiatry, vol. 34, no. 1, 2010, pp. 50-6.
Zai CC, Tiwari AK, Basile V, et al. Oxidative stress in tardive dyskinesia: genetic association study and meta-analysis of NADPH quinine oxidoreductase 1 (NQO1) and Superoxide dismutase 2 (SOD2, MnSOD) genes. Prog Neuropsychopharmacol Biol Psychiatry. 2010;34(1):50-6.
Zai, C. C., Tiwari, A. K., Basile, V., de Luca, V., Müller, D. J., Voineskos, A. N., Remington, G., Meltzer, H. Y., Lieberman, J. A., Potkin, S. G., & Kennedy, J. L. (2010). Oxidative stress in tardive dyskinesia: genetic association study and meta-analysis of NADPH quinine oxidoreductase 1 (NQO1) and Superoxide dismutase 2 (SOD2, MnSOD) genes. Progress in Neuro-psychopharmacology & Biological Psychiatry, 34(1), 50-6. https://doi.org/10.1016/j.pnpbp.2009.09.020
Zai CC, et al. Oxidative Stress in Tardive Dyskinesia: Genetic Association Study and Meta-analysis of NADPH Quinine Oxidoreductase 1 (NQO1) and Superoxide Dismutase 2 (SOD2, MnSOD) Genes. Prog Neuropsychopharmacol Biol Psychiatry. 2010 Feb 1;34(1):50-6. PubMed PMID: 19778569.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress in tardive dyskinesia: genetic association study and meta-analysis of NADPH quinine oxidoreductase 1 (NQO1) and Superoxide dismutase 2 (SOD2, MnSOD) genes. AU - Zai,Clement C, AU - Tiwari,Arun K, AU - Basile,Vincenzo, AU - de Luca,Vincenzo, AU - Müller,Daniel J, AU - Voineskos,Aristotle N, AU - Remington,Gary, AU - Meltzer,Herbert Y, AU - Lieberman,Jeffrey A, AU - Potkin,Steven G, AU - Kennedy,James L, Y1 - 2009/09/22/ PY - 2009/07/06/received PY - 2009/09/16/revised PY - 2009/09/16/accepted PY - 2009/9/26/entrez PY - 2009/9/26/pubmed PY - 2010/4/8/medline SP - 50 EP - 6 JF - Progress in neuro-psychopharmacology & biological psychiatry JO - Prog Neuropsychopharmacol Biol Psychiatry VL - 34 IS - 1 N2 - INTRODUCTION: Tardive dyskinesia (TD) is a potentially irreversible side effect of antipsychotic medication treatment that occurs in approximately 25% of chronically treated schizophrenia patients. Oxidative stress has been one of the proposed mechanisms influencing TD risk. Pae et al. (2004) originally reported a significant association between TD and the NADPH quinine oxidoreductase 1 (NQO1) gene Pro187Ser (C609T, rs1800566) polymorphism in Korean schizophrenia patients; however, subsequent studies have not consistently replicated these findings. Similarly, Hori et al. (2000) reported an association between TD and the Manganese superoxide dismutase SOD2 (MnSOD) gene Ala9Val (rs4880) polymorphism in a Japanese sample, but most research groups failed to replicate their positive findings. AIMS: We investigated the role of the NQO1 polymorphism Pro187Ser and SOD2 (Ala9Val) in a group of well-characterized schizophrenia patients (N=223) assessed for TD. We also performed a meta-analysis of all the previously published TD studies, including data from our sample, on these polymorphisms, Pro187Ser (N=5 studies) and Ala9Val (N=9 studies). RESULTS: We did not observe a significant association of the Pro187Ser or Ala9Val polymorphism with TD occurrence or AIMS scores in our Caucasian and African American samples when analyzed independently. Meta-analysis did not reveal a significant association of the Pro187Ser/Ala9Val alleles or genotypes with TD occurrence. CONCLUSIONS: Neither the NQO1 Pro187Ser nor the SOD2 Ala9Val appear to play a major role in TD risk, although additional polymorphisms should be tested before the role of NQO1 and SOD2 in TD can be completely excluded. SN - 1878-4216 UR - https://www.unboundmedicine.com/medline/citation/19778569/Oxidative_stress_in_tardive_dyskinesia:_genetic_association_study_and_meta_analysis_of_NADPH_quinine_oxidoreductase_1__NQO1__and_Superoxide_dismutase_2__SOD2_MnSOD__genes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0278-5846(09)00320-0 DB - PRIME DP - Unbound Medicine ER -