Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This research is designed to evaluate a number of biological markers to estimate harmful exposure on coal miners from different mining regions in France and to relate the outcome to differences in prevalence of coal worker pneumoconiosis (CWP) between these regions. Eight epidemiological groups of active and ex-miners (smokers and non-smokers) have been selected in the French collieries (North, Lorraine and Provence) according to their occupational and pneumoconiotic status. The following biomarkers have been evaluated: cellularity of sputum, elementary analysis of particles in TEM/EDAX, plasma neutral metalloendo-peptidase elastase type (NMEP), leucocyte elastase (HLE), fibronectin (FN) and elastin peptides. Pulmonary alveolitis, expressed by sputum cellularity, is different between active workers groups but not related to the general background of pneumoconiosis prevalence in the French collieries. In the plasma parameters, fibronectin, HLE and NMEP significantly increased in all groups of coal mine workers as compared to the control group, except for fibronectin parameter in Lorraine collierie. The degree of increase of these parameters allow us to discriminate the different groups and suggest that plasma FN, HLE and NMEP may be considered as biological markers of chronic inhalation of coal mine dust particles. The decrease of elastin peptides level in the Lorraine group alone suggests a specific alteration of elastin metabolism. These parameters were not related to the development of pneumoconiosis and its degree of severity.
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PMID:Biological markers as indicators of exposure and pneumoconiotic risk: prospective study. 840 28

After isolation, purification, and radiolabeling of elastin from baboon aorta and lung, the rates of hydrolysis of both 3H-labeled elastins by porcine pancreatic elastase (PPE or by human leukocyte elastase (HLE) were compared. PPE (30 nM) degraded aorta and lung elastins at rates of 40 and 75 micrograms/h, respectively, leading to their complete solubilization. In contrast, the low rate of hydrolysis of lung elastin (10 micrograms/h) by HLE was paradoxically accompanied with a fivefold decrease in the Michaelis constant value and became negligible after 1 h of incubation. Moreover, HLE adsorption isotherms showed that 0.87 nmol HLE was adsorbed on 1 mg of aorta elastin vs. 1.30 nmol/mg lung elastin. Also, increasing ionic strength was found to enhance the elastolytic potential of HLE toward lung elastin. Investigations were carried out to explain why baboon lung elastin exhibited low susceptibility to hydrolysis by HLE. Solubilization of lung elastin with PPE produced a residue that exhibited inhibitory capacity toward HLE when either 3H-labeled aorta elastin or succinyl trialanine nitroanilide was used as a substrate. When analyzed by transmission electron microscopy, this residue was found to consist of several mineral dust particles, mainly kaolinite (53%) of environmental origin. The HLE-inhibitory capacities of various mineral or coal mine dust particles were then analyzed. Mineral aluminium-silicate dusts were found to be potent HLE inhibitors: 5 micrograms of either kaolinite or montmorillonite totally abolished the activity of 0.45 micrograms of HLE. All these results allowed us to propose that HLE inhibition by aluminium-silicate dusts may be of importance in the pathogenesis of industrial pneumoconiosis and in opportunistic lung infections.
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PMID:Inhibition of human leukocyte elastase by mineral dust particles. 896 10