| Genetic Polymorphism of Epoxide Hydrolase and GSTM1 in Chronic Obstructive Pulmonary Disease. |
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Sang Sun Park, Eun Joung Kim, Chang Young Son, Jeong Ook Wi, Kyung Hwa Park, Gye Jung Cho, Jin Young Ju, Kyu Sik Kim, Yu Il Kim, Sung Chul Lim, Young Chul Kim, Kyung Ok Park, Kook Joo Na |
1Department of Internal Medicine and Thoracic, Chonnam National University Medical School, Gwangju, South Korea. kyc0923@jnu.ac.kr
2Department of Internal Medicine and Cardiovascular Surgery, Chonnam National University Medical School, Gwangju, South Korea. |
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| Abstract |
BACKGROUND
Although smoking is a major cause of chronic obstructive pulmonary disease (COPD), only 10-20% of cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in the activities of the enzyme that detoxify hazardous chemical products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase M1 subunit (GSTM1) genes. METHODS: The genotypes of 58 patients with COPD, and 79 age matched control subjects, were determined by a polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX, and multiplex PCR for the GSTM1. RESULTS: GSTM1 was deleted in 53.3% of the subjects. There was no difference in GSTM1 deletion rates between the COPD patients (32/58, 55.2%) and the control subjects (41/79, 51.9%). The combination patterns of two polymorphisms of mEPHX showed slow enzyme activity in 29(21.2%), normal in 73(53.3%) and fast in 32(23.4%). The COPD group (7/57, 12.3%) showed a significantly lower incidence of slow enzyme activity compared to the control subjects (22/77, 28.6%, p<0.05). However, when the COPD and control groups were compared with smokers only, there were no significant differences in the genotypes of GSTM1 and mEPHX. CONCLUSION: The genotypes of GSTM1 and mEPHX were not significant risk factors of COPD in this cohort of study. |
| Key Words:
COPD, mEPHX, GSTM1 |
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