Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum activities of two lysosomal enzymes, beta-N-acetylglucosaminidase (EC 3.2.1.30; NAG) and beta-glucuronidase (EC 3.2.1.31; GLU) were analysed in 116 male patients with silicosis. Twenty-eight of the patients were matched with controls of similar sex, age and exposure to silica dust but with no radiographical evidence of silicosis. A control group which had not been exposed to silica dust consisted of male blood donors. The mean activity of NAG in serum was higher in the silicosis patients than in the blood donors (P less than 0.01). Similarly, the NAG level in the silicosis patients with matched controls was higher than that in the silica-exposed controls (P less than 0.05). The silicosis patients who showed a progression of small opacities by one or more subcategories had a slightly higher mean NAG activity in their sera than the patients with no progression but this difference did not reach statistical significance; the activity was higher than in silica-exposed controls (P less than 0.05). We suggest that these findings may be related to the effects of silica on macrophages which have been observed experimentally in vitro and in vivo and might indicate an increased turnover of macrophages caused by silica dust and active, progressive silicotic fibrosis.
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PMID:Serum beta-N-acetylglucosaminidase and beta-glucuronidase activities in silicosis patients and in workers exposed to silica dust. 633 85

The serum activities of two lysosomal enzymes, beta-N-acetylglucosaminidase (EC 3.2.1.30) and beta-glucuronidase (EC 3.2.1.31) were analyzed for 28 silicosis and 34 asbestosis patients. The enzyme activities of the patients were compared with those of age-, sex- and exposure-matched controls with no radiological signs of pneumoconiosis, and with an additional reference group of blood donors. The serum activity of beta-N-acetylglucosaminidase was higher in the silicosis patients (32.5 +/- 11.7 U/l) than in the asbestosis patients (21.7 +/- 7.9 U/l, p less than 0.001), in the silica exposed controls (27.1 +/- 6.7 U/l, p less than 0.05) or in the blood donors (24.8 +/- 6.3 U/l, p less than 0.05). No significant differences were found in the serum activity of beta-glucuronidase in the studied groups. Although the mechanisms causing different levels of serum beta-N-acetylglucosaminidase activity in silicosis and asbestosis patients remain unresolved, they may be related to the different mechanisms of action of the two dusts on lung (10).
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PMID:Serum lysosomal enzyme activities in silicosis and asbestosis. 684 Feb 31

Inhalation of crystalline silica results in pulmonary fibrosis and silicosis. It has been suggested that mast cells play a role in these conditions. How mast cells would influence pathology is unknown. We thus explored mast cell interactions with silica in vitro and in B6.Cg-kit(W-sh) mast cell-deficient mice. B6.Cg-kit(W-sh) mice did not develop inflammation or significant collagen deposition after instillation of silica, while C57Bl/6 wild-type mice did have these findings. Given this supporting evidence of a role for mast cells in the development of silicosis, we examined the ability of silica to activate mouse bone marrow-derived mast cells (BMMC), including degranulation (beta-hexosaminidase release); production of reactive oxygen species (ROS) and inflammatory mediators; and the effects of silica on Fc epsilon RI-dependent activation. Silica did not induce mast cell degranulation. However, TNF-alpha, IL-13, monocyte chemotactic protein-1, protease activity, and production of ROS were dose-dependently increased after silica exposure, and production was enhanced after Fc epsilon RI stimulation. This mast cell activation was inhibited by anti-inflammatory compounds. As silica mediates some effects in macrophages through scavenger receptors (SRs), we first determined that mast cells express scavenger receptors; then explored the involvement of SR-A and macrophage receptor with colleagenous structure (MARCO). Silica-induced ROS formation, apoptosis, and TNF-alpha production were reduced in BMMC obtained from SR-A, MARCO, and SR-A/MARCO knockout mice. These findings demonstrate that silica directs mast cell production of inflammatory mediators, in part through SRs, providing insight into critical events in the pathogenesis and potential therapeutic targets in silicosis.
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PMID:Silica-directed mast cell activation is enhanced by scavenger receptors. 1690 92