ABSTRACT.We evaluated the possible influence of glutathione S-transferase mu (GSTM1) and glutathione S-transferase theta (GSTT1) genes on genetic damage due to occupational exposure, which contributes to accelerate ageing. This study was conducted on 120 car auto repair workshop workers exposed to occupational hazards and 120 controls without this kind of exposure. The null and non-null genotypes of GSTM1 and GSTT1 genes were determined by multiplex PCR. Micronucleus frequency, Comet tail length and relative telomere length differences between the null and non-null genotypes of the GSTM1 gene were significantly greater in the exposed group. Lack of GSTT1 did not affect the damage biomarkers significantly (P > 0.05), while lack of GSTM1 was associated with greater susceptibility to genomic damage due to occupational exposure. It was concluded that early ageing is under the influence of these genes and the environmental and sociodemographic factors. Duration of working time was significantly associated with micronucleus frequency, Comet tail length and relative telomere length.
The aim of the present study was to determine the phenotype and genotype frequency of the most common β-globin mutations among the thalassemia major (TM) patients, using high-resolution melting (HRM) curve analysis as a novel, reliable and rapid scanning method. In this descriptive-analytical study, real time polymerase chain reaction (PCR) was applied besides HRM assay in the same reaction tube for mutation detection by melting curve behavior analysis of EvaGreen™ dye. The phenotypic and genotypic frequency of β-globin mutations between 120 patients including IVS-II-1(G-A), IVS-I-110 (G-A), IVS-I-5(G-C), FSC 8/9, FSC 36/37, Codon 30, IVS-I-6 (T-C) and IVS-I-1(G-A) was successfully detected. TM patients showed significant genotype heterogeneity. The clinical outcomes of our TM patients were mostly explained by the genotypes linked to the β 0 type of β-tahalssemia. Genotypic analysis showed 70 patients with homozygous mutations TM (40 β 0 / β 0 and 30 β + / β +) and 15 with compound heterozygous TM (14 β + / β 0 and 1 β 0 /Hb Variant). HRM method as a simpler and cost effective way, accurately characterized the molecular basis of the TM patients.
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