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)

A quantitative study of alpha-1-antirypsin and alpha-2-macroglobulin in the sputum showed an increase in both during attacks of asthma and in patients with chronic obstructive bronchitis. The levels were much lower in asthma patients during remissions, in emphysema and in patients with chronic simple bronchitis, without associated bronchospasm. The parallel variations in levels of alpha-1-antitrypsin, albumin and transferrin in the sputum, contrasts with the course of secretory IgA and are in favour of a transudation process of alpha-1-antitrypsin across the respiratory mucosa.
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PMID:[Quantitative study of alpha 1 antitrypsin and alpha 2 macroglobulin in the sputum]. 5 36

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

The lungs of cigarette smokers are known to contain increased concentrations of extracellular ferritin-bound iron. Reductants present in cigarette smoke may mobilize alveolar ferritin-bound iron, which could then promote oxidative injury to lung cells. Because iron-mediated oxidative injury may be relevant to the pathogenesis of emphysema and lung cancer, which have a predilection for upper lobes, we sought to determine whether concentrations of extracellular iron, ferritin, and transferrin differed in upper and lower lobes of cigarette smokers. Bronchoalveolar lavage (BAL) was performed in the upper and lower lobes of 15 asymptomatic smokers and six healthy nonsmokers. BAL fluid recovered from upper lobes of smokers contained higher concentrations of iron (p < 0.01) and ferritin (p < 0.006) and lower concentrations of transferrin (p < 0.003) compared with the lower lobes. In contrast, BAL fluid recovered from upper and lower lobes of nonsmokers contained much lower concentrations of iron and ferritin, and concentrations were similar in both sites. These findings indicate that, compared with the lower lobes, upper lobes of the lungs of smokers contain higher extracellular concentrations of ferritin-bound iron and decreased concentrations of transferrin. This distribution of lung iron and iron-binding proteins may promote oxidative injury in the upper lobes of smokers.
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PMID:Regional variation in iron and iron-binding proteins within the lungs of smokers. 861 66

Free iron in lung can cause the generation of reactive oxygen species, an important factor in chronic obstructive pulmonary disease (COPD) pathogenesis. Iron accumulation has been implicated in oxidative stress in other diseases, such as Alzheimer's and Parkinson's diseases, but little is known about iron accumulation in COPD. We sought to determine if iron content and the expression of iron transport and/or storage genes in lung differ between controls and COPD subjects, and whether changes in these correlate with airway obstruction. Explanted lung tissue was obtained from transplant donors, GOLD 2-3 COPD subjects, and GOLD 4 lung transplant recipients, and bronchoalveolar lavage (BAL) cells were obtained from non-smokers, healthy smokers, and GOLD 1-3 COPD subjects. Iron-positive cells were quantified histologically, and the expression of iron uptake (transferrin and transferrin receptor), storage (ferritin) and export (ferroportin) genes was examined by real-time RT-PCR assay. Percentage of iron-positive cells and expression levels of iron metabolism genes were examined for correlations with airflow limitation indices (forced expiratory volume in the first second (FEV1) and the ratio between FEV1 and forced vital capacity (FEV1/FVC)). The alveolar macrophage was identified as the predominant iron-positive cell type in lung tissues. Furthermore, the quantity of iron deposit and the percentage of iron positive macrophages were increased with COPD and emphysema severity. The mRNA expression of iron uptake and storage genes transferrin and ferritin were significantly increased in GOLD 4 COPD lungs compared to donors (6.9 and 3.22 fold increase, respectively). In BAL cells, the mRNA expression of transferrin, transferrin receptor and ferritin correlated with airway obstruction. These results support activation of an iron sequestration mechanism by alveolar macrophages in COPD, which we postulate is a protective mechanism against iron induced oxidative stress.
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PMID:Increased iron sequestration in alveolar macrophages in chronic obstructive pulmonary disease. 2478 52