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smoking is the major causal factor in the development of chronic
obstructive pulmonary disease (COPD), only 10-20% of chronic heavy
cigarette smokers develop symptomatic COPD which suggests the presence
of genetic susceptibility. This genetic susceptibility to COPD might
depend on variations in enzyme activities that detoxify cigarette smoke
products such as microsomal epoxide hydrolase (mEPHX) and glutathione-S
transferase (GST). As there is increasing evidence that several genes
influence the development of COPD, multiple gene polymorphisms should
be investigated to find out the genetic susceptibility to COPD.
METHODS—The genotypes of 83 patients with COPD and 76 healthy smoking control subjects were determined by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX gene, and multiplex PCR for GST M1 and GST T1 genes. The frequencies of polymorphic genotypes of mEPHX, GST M1, and GST T1 genes were compared both individually and in combination in patients with COPD and healthy smokers.
RESULTS—No differences were observed in the frequency of polymorphic genotypes in exons 3 and 4 of mEPHX, GST M1, and GST T1 genes between patients with COPD and healthy smokers. The frequencies of any combination of these genotypes also showed no differences between the COPD group and the control group.
CONCLUSIONS—Genetic polymorphisms in mEPHX, GST M1, and GST T1 genes are not associated with the development of COPD in Koreans.