PURPOSE: Cigarette smoking is the major risk factor for developing COPD. Cigarette smoke contains massive amount of oxidants. Systemic and local increases in oxidants and decreases in antioxidants have been observed in smokers and individuals with COPD. Reactive oxygen species (ROS) are proposed to be a major cause of the cell and tissue damange. A few genetic variants, mostly in the forms of single nucleotide polymorphisms (SNP) were detected in genes that are directly implicated against oxidative stress. We hypothesized that developing COPD may be associated with SNPs of antioxidant-related genes.
METHODS: SNP and deletion variants of GSTM1 GSTT1, GSTP (Ile105Val), CAT1 (−262 Ñ/T, 1167 Ñ/Ò), GPX1 (Pro197Leu), NQO1 (609C/T) were investigated in COPD patient (N=320) and healthy individuals (N=422) from Republic Bashkortostan (Ufa) by PCR-RLFP method.
RESULTS: Analysis of the CAT gene variants (−262 Ñ/T, 1167 Ñ/Ò) revealed statistically significant differences in the haplotype frequency distributions between COPD and control group (X2=9.39 P=0.049). The patients with COPD the showed elevated frequency of the CT-CC haplotype (22.41% vs 16.12%; X2=2.29 P=0.11). The genotype frequency distributions of the GSTP gene was significantly differed between COPD and control group (X2=4.62 P=0.05). But at the same time we did not find any differences in the genotype frequency distributions of the GSTM1 GSTT1 GPX1 and NQO1genes within the patients and healthy groups. The distribution of the antioxidant-related genes genotypes did not significantly differ between patients with radiological emphysema and patients without emphysema.
CONCLUSION: Based on the reported data, it is concluded that CAT and GSTP1 genes variants probably play a substantial part in susceptibility to COPD.
CLINICAL IMPLICATIONS: These genetic markers might be helpful inchoosing the adequate therapeutic measures, including antioxidant therapy of COPD exacerbations.
DISCLOSURE: Gulnaz Korytina, None.