Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.5 (cathepsin D)
 4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dynamics of the biological response of pulmonary tissue to silica dust (silica earth from Piotrowice, Poland, recommended as a domestic reference fibrogenic standard) was studied in rats after single-shot intratracheal instillation of a suspension of 20 mg of the dust for one, three, and seven months. Silica dust provoked pronounced pulmonary fibrosis as inferred from increased collagen content together with pathomorphological alteration (silicotic nodules). The lung burden of silica dust affected the lysosomal subfraction as manifested by an increase in its protein content with concomitant stimulation (release and presumably induction) of beta-glucuronidase and cathepsin D and a transient (up to three months) stimulation of lipid peroxidation. Stimulation of activity of lysosomal enzymes and lipid peroxidation mediated by silica dust may reflect destructive metabolic processes resulting in the development of pulmonary fibrosis as the sign of a pathological repair mechanism. The extent of the effects brought about by silica earth testify that it may be recommended as a reference standard for evaluating the potential health hazard from industrial exposure to dusts containing SiO2.
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PMID:Silica earth provoked lung fibrosis with stimulation of lysosomal enzymes and lipid peroxidation in rats. 283 69

Guinea pigs were exposed to silica dust (SiO2) aerosols at 6, 13, 28, and 46 mg/m3 for 3 weeks and examined 4, 8, 16, and 23 weeks later. Twenty-four milligrams of TiO2 per cubic meter served as the control dust. Lung weights were increased at 8 weeks and later. Free lung cells showed a tendency to decrease in phagocytosis capacity at 8 weeks after cessation of exposure and later. Alveolar macrophage production of N-acetyl-beta-D-glucosaminidase, cathepsin D, and acid phosphatase was decreased at 8 weeks after exposure and later. The relationship between the depressant effect on macrophages and the absence of an exposure-related polymorphonuclear neutrophil response for the development of fibrosis could be part of the mechanism behind fibrosis.
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PMID:Pulmonary macrophage phagocytosis and enzyme production after in vivo exposure to silica dust. 630 49