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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elastolytic enzymes and active oxygen species derived from leukocytes and alveolar macrophages during exposure to tobacco smoke, together with active oxygen species directly derived from tobacco smoke, are thought to play a crucial role in the pathogenesis of pulmonary emphysema by inactivating alpha 1 protease inhibitor (alpha 1 PI), a novel anti-elastase. We studied the inhibitory effect of probucol, an oral hypocholesterolemic agent, on tobacco smoke-induced decrease in plasma anti-elastase activity (EIA) and ferroxidase activity (FA) in conscious venous catheter instrumented rats. Rats exposed to the smoke of 5 cigarettes (nicotine 11 mg, tar 115 mg) in a plastic chamber showed a prompt increase in plasma COHb to 17.9 +/- 2.7%, and a prompt decrease in plasma EIA by -17.9% (p less than 0.05) and FA by -14.8% (p less than 0.01), which lasted for 6 hours after exposure. Rats administered probucol (1% probucol in food) for 3 days showed normal cholesterol plasma levels, and rats administered probucol for 4 weeks showed hypocholesterolemic plasma levels. EIA and FA were not depressed after smoking, and lipid peroxide product (TBA reactive substance) in lung tissue (p less than 0.05) and serum (p less than 0.1) showed a smaller increase in association with a smaller decrease in the ratio of lung tissue GSH/GSSG (p less than 0.01) compared with control rats. These results indicate that probucol, via its antioxidant action rather than its cholesterol lowering effect, has a protective effect on lung exposed to tobacco smoke in terms of protease-antiprotease balance and oxidant-antioxidant balance.
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PMID:[Probucol inhibits tobacco smoke-induced decrease in plasma anti-elastase activity and ferroxidase activity in rats]. 140 72

Highly reactive molecules called free radicals can cause tissue damage by reacting with polyunsaturated fatty acids in cellular membranes, nucleotides in DNA, and critical sulfhydryl bonds in proteins. Free radicals can originate endogenously from normal metabolic reactions or exogenously as components of tobacco smoke and air pollutants and indirectly through the metabolism of certain solvents, drugs, and pesticides as well as through exposure to radiation. There is some evidence that free radical damage contributes to the etiology of many chronic health problems such as emphysema, cardiovascular and inflammatory diseases, cataracts, and cancer. Defenses against free radical damage include tocopherol (vitamin E), ascorbic acid (vitamin C), beta-carotene, glutathione, uric acid, bilirubin, and several metalloenzymes including glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc, manganese) and proteins such as ceruloplasmin (copper). The extent of tissue damage is the result of the balance between the free radicals generated and the antioxidant protective defense system. Several dietary micronutrients contribute greatly to the protective system. Based on the growing interest in free radical biology and the lack of effective therapies for many of the chronic diseases, the usefulness of essential, safe nutrients in protecting against the adverse effects of oxidative injury warrants further study.
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PMID:Free radical tissue damage: protective role of antioxidant nutrients. 331 7

Serum levels of ceruloplasmin were investigated in 20 patients with severe chronic airflow obstruction (CAO) and emphysematous changes, but in whom no acute exacerbation was present. For comparison, 20 age- and sex-matched controls with a similar current tobacco consumption were investigated. Also 20 age- and sex-matched non-smoking controls were investigated. Ceruloplasmin was assessed by rocket immuno-electrophoresis, haptoglobin and orosomucoid by a laser-nephelometric method. Patients were selected on grounds of spirometric values; the reversibility test for isoprenaline was performed. Diffusing capacity was used as a measure for emphysematous lesions. Ceruloplasmin levels were found to be significantly elevated in patients with CAO, as compared with smoking and non-smoking control groups. There was no correlation between patients' current tobacco consumption and ceruloplasmin level. The other two acute phase reactants, haptoglobin and orosomucoid, were normal. It is suggested that the increased ceruloplasmin in CAO is a measure of antioxidant activity, which may play a part in the pathogenesis of pulmonary emphysema.
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PMID:Increased serum levels of ceruloplasmin in severe chronic airflow obstruction. 356 44

We investigated the concentration of ceruloplasmin (CP), transferrin (T) and metal ions (Cu, Zn) in serum of healthy smokers, emphysema patients and healty non-smoking subjects (control). We observed elevated Cu concentration in smokers and emphysema patients. Elevated CP concentration was observed only in those emphysema patients who smoked cigarettes, but not in healthy smokers. This observation excludes the possibility of compensative CP and Cu increase as the effect of chronic oxidant exposure. Changes in concentration of CP and Cu observed by us are probably due to chronic inflammation of respiratory tract not only of emphysema patients but also of chronic smokers without signs of the disease.
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PMID:[Evaluation of selected factors induced by antioxidative activity in serum of cigarette smokers and in patients with early phase emphysema]. 764 36

Bronchopulmonary dysplasia is a most frequent contemporary lesion of the lung in early childhood. It is characterized by clinical symptoms (neonatal respiratory distress syndrome) and by X-ray picture reflecting progressive morphological changes in the respiratory tract, i.e. in trachea, bronchi, bronchioles, and pulmonary acini, followed by interstitial pulmonary lesion. As usual, bronchopulmonary dysplasia is forerun by hyaline membranes and may be associated with or followed by interstitial emphysema. Pathogenetic participants are toxicity of highly concentrated and long administered oxygen, artificial mechanical ventilation with an intermittently positive pressure, barotrauma first of immature lung causing emphysema and pneumothorax and pneumomediastinum, lung edema, shortage of A and E vitamins and ceruloplasmin deficiency. Morphological changes in bronchopulmonary dysplasia are alike diffuse alveolar damage in bigger children or adults. Nevertheless, neonatal changes differ from later pulmonary lesion by evolving in an immature tissue and by being complicated with necrotizing "obstructive" bronchiolitis.
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PMID:[Bronchopulmonary dysplasia]. 833 23