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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
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: [email protected]

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.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2012

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