Ankara Universitesi Eczacilik Fakultesi Dergisi, cilt.45, sa.1, ss.41-56, 2021 (Scopus)
© 2021 University of Ankara. All rights reserved.Objective: The aim of this study the investigation of "null" alleles in GSTM1 and GSTT1 gene regions in the development of COPD disease. Material and Method: There are 36 patients with COPD and 14 control cases, who received the Ethics Committee permission from Polatli Duatepe State Hospital Chest Diseases Department. DNA isolations were made from blood samples from the end of 2019 and the control group. Deletions in GSTM1 and GSTT1 gene regions were examined by qPCR method in COPD patient and control groups. The results of the study were evaluated comparatively by distributing the gene dose according to the Hardy-Weinberg. Result and Discussion: When seen from 36 COPD patients after qPCR analysis, it was found that deletion expressions due to gene doses in all patient groups; 23 individuals (63.8%) in the (+/-) genotype for GST-M1, 13 individuals (26.2%) in the (-/-) genotype. For GST-T1, 14 (%) in the (+/+) genotype 38.8), while deletion was observed with the highest rate, 4 individuals (11.1%) in the (+/-) genotype and 18 individuals (50.1%) in the (-/-) genotype were found. For GST-M1, deletion was observed in 19 individuals (63.3%) in the genotype (+/-) in male individuals, while it was observed in 4 individuals (66.6%) with the same genotype in women. While deletion was not observed in 11 (36.6%) male patients, this rate was observed as 2 (33.4%) in women. In the GST-T1 gene region, there were 10 (33.3%) males in male patients and 4 (66.6%) individuals in female patients with deletion occurring and the frequency of the "null allele" was high (+/+). In the (+/-) genotype, 3 (10%) in males and 1 (16.7%) in females were found. In the genotype where deletion was not observed and the gene was conserved (-/-), 17 (56.7%) individuals were observed in male patients and 1 (16.7%) in female patients. In the case that the gene "null" allele status in the GST-M1 gene region is slightly higher than the GST-T1 gene communication, this situation is thought to be a factor in obstructive pulmonary disease.