Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of angiotensin-converting enzyme (ACE) in people with extrinsic allergic alveolitis (EAA) have been both increased and decreased. These observations suggest that pulmonary macrophages or endothelial cells participate in the disease process. Exposure to molds in the tobacco industry has recently been suspected to be associated with chronic extrinsic allergic alveolitis. In the present study, we analyzed the serum activities of ACE and two lysosomal enzymes, beta-N-acetylglycosaminidase (NAG) and beta-glucuronidase (GLU), among 57 tobacco workers. The tobacco workers not exposed had serum ACE levels similar to those of the reference population workers not occupationally exposed to dust (N = 127). The tobacco workers' serum levels of NAG (16.0 +/- 2.0 units/L and GLU (2.4 +/- 0.7 units/L) were higher than among the referents (NAG, 9.1 +/- 2.0 units/L; GLU, 1.0 +/- 0.6 units/L; p less than 0.01). Fifteen tobacco workers with respiratory symptoms compatible with pulmonary diseases caused by organic dust had a trend toward increased ACE, NAG, and GLU levels. The mean level of ACE in serum was higher among the workers with (25.8 +/- 4.5 units/L) than among those without pulmonary fibrosis (20.7 +/- 7.5 units/L; p less than 0.025). The mean ACE level was also higher among workers with the highest exposure to molds (24.6 +/- 7.1 units/L) compared to those with the mildest exposure (18.3 +/- 5.7 units/L; p less than 0.05). Tobacco workers with or without antibodies against one or more microbes had similar mean levels of ACE, NAG, and GLU. All of these findings indicate that raw tobacco dust and its contaminants may cause allergic or toxic reactions or both, reflected by the serum levels of ACE, NAG, and GLU.
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PMID:Serum angiotensin-converting enzyme and lysosomal enzymes in tobacco workers. 300 24

Hydrolytic enzymes [acid phosphatase, beta-glucuronidase, beta-D-N-acetyl glucosaminidase (beta-D-NAGA), lysozyme and angiotensin-converting enzyme (ACE)] are the major constituents of alveolar macrophages (AM). These enzymes play a crucial role in the pathogenesis of interstitial lung diseases. Cell-associated activity of several enzymes in alveolar macrophages obtained from control subjects (n = 5) and patients suffering five representative types of interstitial pulmonary diseases [sarcoidosis (n = 10), extrinsic allergic alveolitis (n = 5), idiopathic pulmonary fibrosis (n = 5), neoplastic infiltration of the lung (n = 5) and Pneumocystis carinii pneumonia (n = 5)] were evaluated. Cells were obtained by bronchoalveolar lavage and isolated by Ficoll-Hypaque gradient. Enzymatic activity was assessed by standardized tests. Bronchoalveolar lavage (BAL) lymphocyte counts were significantly elevated in the patients with active sarcoidosis (median: 57%), allergic extrinsic alveolitis (median: 51%) and neoplastic infiltration (median: 31%) as compared with the other groups, whereas BAL neutrophil and eosinophil counts were significantly elevated in the patients with idiopathic pulmonary fibrosis (neutrophil median: 29%; eosinophil median: 3%). The highest alveolar macrophage enzymatic activities were obtained in the active sarcoidosis group (median ACE: 23.38 microKat 10(-6) AM; median lysozyme: 8.64 nKat 10(-6) AM; median beta-glucuronidase: 324.22 U 10(-6) AM; median acid phosphatase: 0.78 nKat 10(-6) AM; median beta-D-NAGA: 1.85 nKat 10(-6) AM) which was significantly greater than in the control group (median ACE: 6.69 microKat 10(-6) AM; median lysozyme: 1.95 nKat 10(-6) AM; median beta-glucuronidase: 39.88 U 10(-6) AM; median acid phosphatase: 0.38 nKat 10(-6) AM; median beta-D-NAGA: 0.44 nKat 10(-6) AM). However, intracellular lysosomal enzymatic activities of alveolar macrophages from patients with allergic extrinsic alveolitis, a disease in which the degree of alveolar macrophage activation is maximal, were similar to those of the control group. These findings demonstrated a different pattern of expression of alveolar macrophage's hydrolytic enzymes in lymphocytic diffuse pulmonary interstitial disease. In sarcoidotic patients, hydrolytic enzymes were increased whereas in allergic extrinsic alveolitis, hydrolytic enzyme activities were similar to control groups. Indirect data suggest that the release of lysosomal enzymes by alveolar macrophages during allergic extrinsic alveolitis may be a factor involved in the pulmonary lesions appearing in this disease.
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PMID:Hydrolytic enzyme of the alveolar macrophage in diffuse pulmonary interstitial disease. 873 8

Several lines of research indirectly suggest that platelet activating factor (PAF) may intervene in the pathogenesis of extrinsic allergic alveolitis (EAA). The specific aim of our study was to evaluate the participation of PAF on macrophage activation during the acute phase of EAA in an experimental model of this disease developed in guinea pigs. Initially we measured the concentration of PAF in bronchoalvedar lavage fluid, blood and lung tissue. In a second phase we evaluate the participation of PAF on alveolar macrophage activation and parenchymal lung injury. The effect of PAF on parenchymal lung injury was evaluated by measuring several lung parenchymatous lesion indices (lung index, bronchoalvedar lavage fluid (BALF) lactic hydrogenase activity and BALF alkaline phosphatase activity) and parameters of systemic response to the challenge (acute phase reagents). We observed that induction of the experimental EAA gave rise to an increase in the concentration of PAF in blood and in lung tissue. The use of the PAF-receptor antagonist BN52021 decreases the release of lysosomal enzymes (beta-glucuronidase and tartrate-sensitive acid phosphatase) to the extracellular environment both in vivo and in vitro. Furthermore, antagonism of the PAF receptors notably decreases pulmonary parenchymatous lesion. These data suggest that lung lesions from acute EAA are partly mediated by local production of PAF.
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PMID:BN 52021 (a platelet activating factor-receptor antagonist) decreases alveolar macrophage-mediated lung injury in experimental extrinsic allergic alveolitis. 1070 58