Neuron Glia Biology · 2011 · 10 citations · 22 references
Life SciencesGeneticsPsychiatryGenetic EpidemiologyHuman GeneticsMedical GeneticsGenetic Risk FactorsGenetic SusceptibilityGenotype-phenotype Association AnalysisGlutathione MetabolismPsychiatric EpidemiologyPsychiatric GeneticsAntioxidantsCase-control Study DesignGenomic Dna AnalysisGlutathione S-transferase ActivityGlutathione S-transferasesMolecular Genetic EpidemiologyPsychiatric Genetic RiskSchizophrenia Genetics
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.
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Human SULT1A1 gene: copy number differences and functional implications
Scott J. Hebbring, Araba A. Adjei, Janel L. Baer et al. · Human Molecular Genetics · 2006 · 110 citations · Full text