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• W2115882316 endingPage "S14" @default.
• W2115882316 startingPage "S10" @default.
• W2115882316 abstract "The first-pass metabolism of foreign compounds in the lung is an important protective mechanism against oxidative stress. We investigated whether polymorphisms in the gene for microsomal epoxide hydrolase (mEPHX), an enzyme involved in this protective process, had any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease (COPD) and emphysema.We designed PCR-based genotyping assays to detect variant forms of mEPHX that confer slow and fast activity. We used these assays to screen 203 blood-donor controls and groups of patients with asthma (n = 57), lung cancer (n = 50), COPD (n = 68), and emphysema (n = 94), who were attending specialised clinics in Edinburgh, UK.The proportion of individuals with innate slow mEPHX activity (homozygotes) was significantly higher in both the COPD group and the emphysema group than in the control group (COPD 13 [19%] vs control 13 [6%]; emphysema 21 [22%] vs 13 [6%]). The odds ratios for homozygous slow activity versus all other phenotypes were 4.1 (95% CI 1.8-9.7) for COPD and 5.0 (2.3-10.9) for emphysema.Genetic polymorphisms in xenobiotic enzymes may have a role in individual susceptibility to oxidant-related lung disease. Epoxide derivatives of cigarette-smoke components may be the cause of some of the lung damage characteristics of these diseases." @default.
• W2115882316 created "2016-06-24" @default.
• W2115882316 creator A5036400895 @default.
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• W2115882316 date "1998-08-01" @default.
• W2115882316 modified "2023-10-18" @default.
• W2115882316 title "Genes, oxidative stress, and the risk of chronic obstructive pulmonary disease" @default.
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• W2115882316 doi "https://doi.org/10.1136/thx.53.2008.s10" @default.
• W2115882316 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1765894" @default.
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• W2115882316 hasPublicationYear "1998" @default.
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