Yim_2002_Lung_180_119

The fact that only 10-20% of chronic heavy cigarette smokers develop symptomatic COPD and correlations of pulmonary function among twins and families suggests the presence of genetic susceptibility in the development of COPD. Genetic susceptibility to COPD might depend on the variations in enzyme activities that detoxify cigarette smoke products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase (GST). The purpose of this study was to determine whether polymorphism of GSTP1 gene is linked to a genetic susceptibility to COPD. The hypothesis we tested here was that the polymorphism supposed to decrease GSTP1 activity would be the genetic risk for the development of COPD. Using PCR followed by restriction fragment length polymorphism (PCR-RFLP), genotypes of Ile105Val polymorphism in exon 5 of glutathione S-transferase P1 (GSTP1) gene were determined in 89 patients with COPD and 94 healthy smoking control subjects at the Seoul National University Hospital. Although the frequency of homozygous wild allele in exon 5 of GSTP1 gene in patients with COPD was higher than that observed in healthy controls (71% vs. 61%), the difference was not considered statistically significant. Neither the heterozygous nor homozygous mutant allele differed in frequency between the two groups. In conclusion, the genetic polymorphisms of exon 5 of GSTP1 gene may not be associated with development of COPD in Koreans.