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Analysis of glutathione S-transferase genes polymorphisms and the risk of schizophrenia in a sample of Iranian population

Published online by Cambridge University Press:  06 July 2012

Farah Lotfi Kashani ,
Dor Mohammad Kordi-Tamandani ,
Roya Sahranavard ,
Mohammad Hashemi ,
Farzaneh Kordi-Tamandani  and
Adam Torkamanzehi
Farah Lotfi Kashani
Affiliation:
Department of Clinical Psychology, Islamic Azad University (Roudehen Branch), Roudehen, Iran
Dor Mohammad Kordi-Tamandani*
Affiliation:
Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran
Roya Sahranavard
Affiliation:
Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran
Mohammad Hashemi
Affiliation:
Department of Clinical Biochemistry, Zahedan University of Medical Sciences, Zahedan, Iran
Farzaneh Kordi-Tamandani
Affiliation:
Department of Psychology, Ferdowsi University of Mashhad, Mashhad, Iran
Adam Torkamanzehi
Affiliation:
Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran
*
Correspondence should be addressed to: Dr. Dor Mohammad Kordi-Tamandani, Department of Biology, University of Sistan and Baluchestan, P.O. Box 98155-987, Zahedan, Iran phone: +98 541 2452335 fax: +98 541 2446565 email: dor_kordi@yahoo.com
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Abstract

Glutathione S-transferases (GSTs) are major intracellular antioxidants, which, impaired in their function, are involved in the progress of schizophrenia (SCZ). The aim of this case-control study was to investigate the association between the polymorphism of glutathione S-transferases M1 (GSTM1), T1 (GSTT1), the glutathione S-transferase P1 gene (GSTP1) and SCZ. We isolated genomic DNA from peripheral blood of 93 individuals with SCZ and 99 healthy control subjects' genotypes analyzing them for GSTM1, GSTT1 and GSTP1 using polymerase chain reaction. The analysis of the gene–gene interaction between GSTs indicated that the magnitude of the association was greater for the combined AG/GSTT1 & GSTM1 genotypes (OR = 2.51; 95% CI: 1.13–5.63, P = 0.02). The AG and combined AG + GG genotypes of GSTP1 increased the risk of SCZ (OR = 1.83; 95% CI: 0.94–3.75 and OR = 1.71; 95% CI: 0.92–3.19, respectively). The genotypes of GSTT/NULL, NULL/GSTM and NULL/NULL increased the risk of SCZ (OR = 2.05; 95% CI: 0.9–4.74; OR = 2.0; 95% CI: 1.68–2.31; and OR = 1.8; 95% CI: 0.57–2.46, respectively). The present study supports previous data that suggest that impairment in the function of GSTs genes may increase the risk of SCZ.

Keywords

GSTM1GSTPGSTTschizophreniapolymorphism
Type
Research Article
Information
Neuron Glia Biology , Volume 7 , Issue 2-4 , May 2011 , pp. 199 - 203
Copyright
Copyright © Cambridge University Press 2012

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References

REFERENCES

Acar, H., Kilinc, M., Guven, S. and Inan, Z. (2011) Glutathione S-transferase M1 and T1 polymorphisms in Turkish patients with varicocele. Andrologia 44, 34–37; doi: i10.1111/j.1439-0272.2010.01103.x.CrossRefGoogle ScholarPubMed
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, 4th edn.Washington, DC: American Psychiatric Association.Google Scholar
Behrens, M.M. and Sejnowski, T.J. (2009) Does schizophrenia arise from oxidative dysregulation of parvalbumin-interneurons in the developing cortex? Neuropharmacology 57, 193–200; doi: iS0028-3908(09)00157-9 [pii] 10.1016/j.neuropharm.2009.06.002.Google Scholar
Benes, F.M., Matzilevich, D., Burke, R.E. and Walsh, J. (2006) The expression of proapoptosis genes is increased in bipolar disorder, but not in schizophrenia. Molecular Psychiatry 11, 241–251.Google Scholar
Berk, M., Ng, F., Dean, O., Dodd, S. and Bush, A.I. (2008) Glutathione: a novel treatment target in psychiatry. Trends in Pharmacological Sciences 29, 346–351.Google Scholar
Bjork, K., Saarikoski, S.T., Arlinde, C., Kovanen, L., Osei-Hyiaman, D., Ubaldi, M. et al. (2006) Glutathione-S-transferase expression in the brain: possible role in ethanol preference and longevity. FASEB Journal 20, 1826–1835; doi: i20/11/1826 [pii] 10.1096/fj.06-5896com.Google Scholar
Csejtei, A., Tibold, A., Varga, Z., Koltai, K., Ember, A., Orsos, Z. et al. (2008) GSTM, GSTT and p53 polymorphisms as modifiers of clinical outcome in colorectal cancer. Anticancer Research 28, 1917–1922.Google ScholarPubMed
Gravina, P., Spoletini, I., Masini, S., Valentini, A., Vanni, D., Paladini, E. et al. (2011) Genetic polymorphisms of glutathione S-transferases GSTM1, GSTT1, GSTP1 and GSTA1 as risk factors for schizophrenia. Psychiatry Research 187, 454–456.Google Scholar
Gysin, R., Kraftsik, R., Sandell, J., Bovet, P., Chappuis, C., Conus, P. et al. (2007a) Impaired glutathione synthesis in schizophrenia: convergent genetic and functional evidence. Proceedings of the National Academy of Sciences of the U.S.A. 104, 16621–16626.Google Scholar
Harada, S., Tachikawa, H. and Kawanishi, Y. (2001) Glutathione S-transferase M1 gene deletion may be associated with susceptibility to certain forms of schizophrenia. Biochemical and Biophysical Research Communications 281, 267–271.Google Scholar
Hebbring, S.J., Adjei, A.A., Baer, J.L., Jenkins, G.D., Zhang, J., Cunningham, J.M. et al. (2007) Human SULT1A1 gene: copy number differences and functional implications. Human Molecular Genetics 16, 463–470.CrossRefGoogle ScholarPubMed
Koizumi, H., Hashimoto, K., Kumakiri, C., Shimizu, E., Sekine, Y., Ozaki, N. et al. (2004) Association between the glutathione S-transferase M1 gene deletion and female methamphetamine abusers. American Journal of Medical Genetics Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics 126B, 43–45.CrossRefGoogle ScholarPubMed
Kordi-Tamandani, D.M., Hashemi, M., Birjandian, E., Bahari, A., Valizadeh, J. and Torkamanzehi, A. (2011a) Lack of association of GSTT1 and GSTP1 genes methylation and their expression profiles with risk of NAFLD in a sample of Iranian patients. Clinics and Research in Hepatology and Gastroenterology 35, 387–392.Google Scholar
Kordi-Tamandani, D.M., Hashemi, M., Sharifi, N., Kaykhaei, M.A. and Torkamanzehi, A. (2011b) Association between paraoxonase-1 gene polymorphisms and risk of metabolic syndrome. Molecular Biology Reports 39, 937–943; doi: i10.1007/s11033-011-0819-x.Google Scholar
Martin, N.J., Collier, A.C., Bowen, L.D., Pritsos, K.L., Goodrich, G.G., Arger, K. et al. (2009) Polymorphisms in the NQO1, GSTT and GSTM genes are associated with coronary heart disease and biomarkers of oxidative stress. Mutation Research 674, 93–100; doi: iS1383-5718(08)00278-7 [pii] 10.1016/j.mrgentox.2008.09.009.Google Scholar
Masoudi, M., Saadat, I., Omidvari, S. and Saadat, M. (2009) Genetic polymorphisms of GSTO2, GSTM1, and GSTT1 and risk of gastric cancer. Molecular Biology Reports 36, 781–784; doi: i10.1007/s11033-008-9245-0.Google Scholar
Mishra, A., Chandra, R., Mehrotra, P.K., Bajpai, P. and Agrawal, D. (2011) Glutathione S-transferase M1 and T1 polymorphism and response to neoadjuvant chemotherapy (CAF) in breast cancer patients. Surgery Today 41, 471–476; doi: i10.1007/s00595-009-4310-4.Google Scholar
Mohammadynejad, P., Saadat, I., Ghanizadeh, A. and Saadat, M. (2011) Bipolar disorder and polymorphisms of glutathione S-transferases M1 (GSTM1) and T1 (GSTT1). Psychiatry Research 186, 144–146.Google Scholar
Pae, C.-U., Kim, J.-J., Lee, S.-J., Lee, C.-U., Lee, C., Paik, I.-H. et al. (2003) Association study between glutathione S-transferase P1 polymorphism and schizophrenia in the Korean population. Progress in Neuro-Psychopharmacology and Biological Psychiatry 27, 519–523.CrossRefGoogle ScholarPubMed
Pemble, S., Schroeder, K.R., Spencer, S.R., Meyer, D.J., Hallier, E., Bolt, H.M. et al. (1994) Human glutathione S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism. Biochemical Journal 300, 271–276.Google Scholar
Rocha, A.V., Talbot, T., Magalhaes da Silva, T., Almeida, M.C., Menezes, C.A., Di Pietro, G. et al. (2011) Is the GSTM1 null polymorphism a risk factor in primary open angle glaucoma? Molecular Vision 17, 1679–1686.Google Scholar
Ross, C.A., Margolis, R.L., Reading, S.A., Pletnikov, M. and Coyle, J.T. (2006) Neurobiology of schizophrenia. Neuron 52, 139–153; doi: iS0896-6273(06)00722-7 [pii] 10.1016/j.neuron.2006.09.015.Google Scholar
Saadat, M., Mobayen, F. and Farrashbandi, H. (2007) Genetic polymorphism of glutathione S-transferase T1: a candidate genetic modifier of individual susceptibility to schizophrenia. Psychiatry Research 153, 87–91; doi: iS0165-1781(06)00100-4 [pii] 10.1016/j.psychres.2006.03.024.Google Scholar
Sharp, A.J., Cheng, Z. and Eichler, E.E. (2006) Structural variation of the human genome. Annual Review of Genomics and Human Genetics 7, 407–442.Google Scholar
Simic, T., Savic-Radojevic, A., Pljesa-Ercegovac, M., Matic, M. and Mimic-Oka, J. (2009) Glutathione S-transferases in kidney and urinary bladder tumors. Nature Reviews. Urology 6, 281–289; doi: inrurol.2009.49 [pii] 10.1038/nrurol.2009.49.Google Scholar
Singh, N., Sinha, N., Kumar, S., Pandey, C.M. and Agrawal, S. (2011) Glutathione S-transferase gene polymorphism as a susceptibility factor for acute myocardial infarction and smoking in the North Indian population. Cardiology 118, 16–21.Google Scholar
Smythies, J. (1999) Redox mechanisms at the glutamate synapse and their significance: a review. European Journal of Pharmacology 370, 1–7.CrossRefGoogle ScholarPubMed
Sullivan, P.F., Kendler, K.S. and Neale, M.C. (2003) Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Archives of General Psychiatry 60, 1187–1192.Google Scholar
Tosic, M., Ott, J., Barral, S., Bovet, P., Deppen, P., Gheorghita, F. et al. (2006) Schizophrenia and oxidative stress: glutamate cysteine ligase modifier as a susceptibility gene. American Journal of Human Genetics 79, 586–592; doi: iS0002-9297(07)62760-8 [pii] 10.1086/507566.Google Scholar
Zeevalk, G.D., Manzino, L., Sonsalla, P.K. and Bernard, L.P. (2007) Characterization of intracellular elevation of glutathione (GSH) with glutathione monoethyl ester and GSH in brain and neuronal cultures: relevance to Parkinson's disease. Experimental Neurology 203, 512–520; doi: S0014-4886(06)00540-1 [pii] 10.1016/j.expneurol.2006.09.004.CrossRefGoogle ScholarPubMed