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)

The air in the Lin-Shen tunnel in Taipei is heavily polluted due to heavy traffic. To elucidate the biologic effects of air pollution, we studied the biochemical alterations of Polycyclic aromatic hydrocarbons metabolic enzymes and histological changes in the livers and lungs in experimental mice under long-term and short-term exposure to the tunnel air. The concentrations of 16 Polycyclic aromatic hydrocarbons in the air were measured by HPLC, and the mutagenicity of the extract of air particulates was assayed by the Ames test. We found that the benzo(a)pyrene hydroxylase and cytochrome P-450 in the livers and nitroreductase in the lungs of the 30-day exposed animals were significantly increased as compared to the unexposed control (p < 0.005). The nitroreductase in the liver also increased but not significantly. The lungs of long-term (6 mo.) exposed mice showed anthracosis, chronic inflammation, and emphysema (10/10). The livers of the experimental animals did not show significant alteration. A whitish circular nodule appeared on the liver surface of one mouse (1/10). Microscopically, the nodule showed necrosis and hyperchromatic cells around the central vein. It is concluded that the polluted air in the traffic tunnel has evident biohazardous effects on the lungs and livers of mice under the experimental conditions.
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PMID:Biochemical and morphological alterations in the lungs and livers of mice following exposure to polluted air in a traffic tunnel. 128 43

3-Methylindole (3MI), an abnormal metabolite of tryptophan, causes acute pulmonary edema and emphysema. 3MI toxicity is species-, tissue- and cell-specific and is an excellent model for understanding the processes of chemically-induced lung injury. Experimental evidence showed that 3MI is metabolically activated by both microsomal cytochrome P-450-dependent mixed function oxidase (MFO) and prostaglandin H synthase (PHS) systems in the lung. Formation of a free radical intermediate during 3MI metabolism is the initial chemical event which is responsible for the pneumotoxicity. 3MI free radicals bind covalently to microsomal protein and induce lipid peroxidation. Microsomal enzymes which regulate the glycogen and phospholipid biosynthesis in the lung are altered during the cellular repair processes after 3MI-induced lung injury. Inhibition of cellular differentiation from Type II to Type I cells and impaired surfactant function may be crucial to the disease process.
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PMID:The metabolic basis of 3-methylindole-induced pneumotoxicity. 218 87

3-Methylindole (3MI), the main ruminal fermentation product of L-tryptophan, causes acute pulmonary edema and interstitial emphysema in ruminants. Intravenous infusion of 3MI in goats causes necrosis and sloughing of pneumocytes and bronchial epithelial cells. Previous studies indicate that a reactive metabolite or metabolites of 3MI bind covalently to tissue macromolecules in the lung and this binding is associated with the pneumotoxicity of 3MI. We undertook this autoradiographic study of 3MI covalent binding to test the hypothesis that reactive 3MI metabolite(s) bind to the lung cells susceptible to 3MI-induced injury. We infused goats with [3H]3MI and killed them either 0.5, 2 or 6 h after start of the infusion. Sections of fixed lung were extensively washed, alcohol dehydrated and embedded in plastic. Only covalently bound radioactivity remained. Silver grains were quantitated per area in the developed autoradiographs. There was a 2:1 ratio of binding to the small airway epithelium compared to the interalveolar septa in all the goats. Both ciliated and non-ciliated bronchiolar cells were labeled, as were both types I and II pneumocytes. Normal goat lung slices incubated in vitro with [3H]3MI were labeled in the same pattern. Inclusion of either of the inhibitors of cytochrome P-450, SKF-525-A or piperonyl butoxide significantly reduced this binding to both the pneumocytes and the bronchiolar cells. We consider these results supportive of our hypothesis that 3MI is metabolized to reactive intermediates by the epithelial cells of the lung, where they bind to macromolecules, which may cause cellular damage.
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PMID:Autoradiographic evidence of 3-methylindole covalent binding to pulmonary epithelial cells in the goat. 620 22