Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk of chronic pulmonary emphysema from exposure to tobacco smoke varies widely from person to person, depending in part on the status of particular genes and acquired susceptibilities. Certain genes determine how cells activate and/or detoxify tobacco smoke products. We aimed to determine whether any genetic susceptibility exists in the development of emphysematous changes confirmed by chest computed tomography (CT). Genotypes of various enzymes involved in the activation or detoxification of tobacco smoke, epoxide hydrolase (EPHX1), cytochrome P450s (CYP1A1 and CYP2E1), glutathione S-transferases (GSTM1/P1/T1), and hemoxygenase-1 (HMOX1), were determined by PCR-based assays in a total of 235 heavy smokers (Brinkman index >/=400). They were divided into two groups according to the CT findings: 63 and 172 subjects with and without emphysematous changes, respectively. Although the allele frequency of any genetic polymorphism was not statistically different between the two groups, the frequency of the individuals having combination of the genotype representing very slow activity for epoxide hydrolase and at least one allele with large size of (GT)n repeats in the HMOX1 gene promoter region was higher in the subjects with emphysematous changes (p=0.03; odds ratio 2.8; 95% CI = 1.07-7.5) among the stratified individuals (age >/=51 years). These findings suggest that combination of several polymorphisms in the enzymes that activate or detoxify the tobacco smoke, such as EPHX1 and HMOX1, might be associated with its affects on the development of emphysematous changes of the lung.
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PMID:Genetic susceptibility for emphysematous changes of the lung in Japanese. 1257 34

Cow dung (Kanda) is a major source of energy in rural and urban population of developing countries and is burnt in traditional open stoves in confined space of kitchen without proper ventilation. In epidemiological studies, biomass fuel smoke has been reported to be responsible for several respiratory disorders in exposed population. In a laboratory experiment, female wistar rats were exposed to kanda smoke for 60 min/day over a period of 12 weeks. Chemical analysis of smoke showed the presence of PAHs. The increase in CYP1A1, GST-ya, GST-yc expression was found in 12 week exposed lung tissues as compared with controls. The exposure to smoke resulted in significant alteration in the BALF cells in the form of clustering of alveolar macrophages and giant cell formation with vacuolated cytoplasm. The macrophages also showed thickness and villi like projections on the cell surface thus reducing their phagocytic activities. Histopathological changes in lung tissue were manifested in the form of damage to bronchiolar epithelium, edema and thickening of alveolar septa and emphysema after 4 and 8 week of exposure. These findings suggest that exposure to kanda smoke increases pulmonary tissue damage and may result in various forms of respiratory infections in the exposed popultion.
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PMID:Multiple approaches to evaluate the toxicity of the biomass fuel cow dung (kanda) smoke. 2171 4