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Relationship between GSTM1 and GSTT1 polymorphisms and schizophrenia: A case-control study in a Tunisian population

Lookup NU author(s): Dr Ramzi LakhdarORCiD

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Abstract

There is substantial evidence found in the literature that supports the fact that the presence of oxidative stress may play an important role in the pathophysiology of schizophrenia. The glutathione S-transferases (GSTs) forms one of the major detoxifying groups of enzymes responsible for eliminating products of oxidative stress. Interindividual differences observed in the metabolism of xenobiotics have been attributed to the genetic polymorphism of genes coding for enzymes involved in detoxification. Thus, in this study we investigated the association of glutathione S-transferase Mu-1 (GSTM1) and glutathione S-transferase theta-1 (GSTT1) gene deletion polymorphisms and schizophrenia in a Tunisian population. A case-control study including 138 schizophrenic patients and 123 healthy controls was enrolled. The GSTM1 and GSTT1 polymorphisms were analyzed by multiplex polymerase chain reaction (PCR). No association was found between the GSTM1 genotype and schizophrenia, whereas the prevalence of the GSTT1 active genotype was significantly higher in the schizophrenic patients (57.2%) than in the controls (45.5%) with (OR = 0.6, IC 0.37-0.99, p=0.039). Thus, we noted a significant association between schizophrenia and GSTT1 active genotype. Furthermore, the combination of the GSTM1 and GSTT1 null genotypes showed a non-significant trend to an increased risk of schizophrenia. The present finding indicated that GSTT1 seems to be a candidate gene for susceptibility to schizophrenia in at least Tunisian population. © 2012 Elsevier B.V.


Publication metadata

Author(s): Raffa M, Lakhdar R, Ghachem M, Barhoumi S, Safar MT, Bel Hadj Jrad B, Haj Khelil A, Kerkeni A, Mechri A

Publication type: Article

Publication status: Published

Journal: Gene

Year: 2013

Volume: 512

Issue: 2

Pages: 282-285

Print publication date: 10/01/2013

Online publication date: 26/10/2012

ISSN (print): 0378-1119

ISSN (electronic): 1879-0038

Publisher: Elsevier

URL: https://doi.org/10.1016/j.gene.2012.10.031

DOI: 10.1016/j.gene.2012.10.031

PubMed id: 23107768


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