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Results for “SILICOSIS”

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At least 1,117 records · Page 62Linked to original sources
PubMed1982

Studies of the chronic toxicity of tetrandrine in dogs: an inhibitor of silicosis.

Dogs administered tetrandrine at low dose (3 mg/kg) and medium dose (10 mg/kg) levels showed no toxic changes. Administration of the drug at a high dose level (40 mg/kg) for 2 months may induce focal necrosis of liver cells, abnormal liver function, and acceleration of erythrocyte sedimentation rate. After the dogs had received tetrandrine for 6 months continuously, necrosis of liver tissue appeared. After continuous administration of tetrandrine, accumulation of the drug in liver, lung, kidney, and adrenal gland was observed. The amount of drug stored in the organs increased with the quantity of drug given to the animal.

Alkaloids↗
PubMed1981

Lactate dehydrogenase isoenzymes in macrophages and serum during the development of pulmonary silicosis in the rat.

The lactate dehydrogenase (LDH) isoenzyme pattern in macrophages (peritoneal and alveolar) in the rat was studied on polyacrylamide gel electrophoresis. Further, the release of LDH isoenzymes from cultured macrophages exposed to silica dust and also the pattern of serum LDH isoenzymes in silica exposed animals were investigated. The isoenzyme pattern of the alveolar macrophages showed all the five bands, contrary to peritoneal macrophages in which two bands, viz. LDH1 and LDH2, were missing. Silica-exposed macrophages liberated LDH5 in the supernatant culture medium. This LDH isoenzyme also increased in the serum of silicotic rats during the early stages of the development of the disease.

Animals↗
PubMed1990

Role of circulating immune complexes in the immunopathogenesis of silicosis.

The sera of 19 silica-dust-exposed subjects and of an equal number of age-, sex- and socioeconomic-strata-matched controls were analysed for antinuclear factor, rheumatoid factor, C-reactive protein, immunoglobulins G, M, A, and complement C3 and C4. Circulating immune complexes were also precipitated in all subjects and their immunoglobulin and complement C3 and C4 were estimated. Silica-exposed subjects were divided into two groups depending upon the radiological findings and it is suggested that IgA plays an important role in the immunopathogenesis of the disease and that lung changes could be due to the immune-complex-mediated mechanisms utilizing an alternative complement pathway.

Adolescent↗
PubMed1986

Regulation of lung fibroblast proliferation and protein synthesis by bronchiolar lavage in experimental silicosis.

Male Sprague-Dawley rats were subjected to a single, intratracheal instillation of 30 mg Min-U-Sil silica in sterile saline and were sacrificed 3, 7, or 14 days following instillation. Control animals were instilled with sterile saline only. Silica instillation produced an inflammatory reaction followed by histological changes characteristic of lung fibrosis. Thickened alveolar septa associated with inflammatory cells transforming into large multifocal fibrotic nodules were detected in silica-exposed animals. Increased numbers of bronchoalveolar cells (principally macrophages), elevated levels of protein (principally serum albumin), and lysozyme, proteolytic (trypsin-like), and myeloperoxidase activities were detected in lavage fluids obtained from animals instilled with silica. These factors (except for lysozyme activity) were elevated above control levels from 3 to 7 days postinstillation and declined to near control levels by Day 14. The rate of DNA, collagen, and noncollagen protein synthesis was significantly elevated in lung tissue minces from silica-treated rats 3 and 7 days after instillation. Elevated levels of total protein, and lung collagen in particular, were observed 9 weeks after insult. Lavage fluid from silica-instilled rats stimulates DNA synthesis in cultures of proliferating and quiescent rat lung fibroblasts. Lavage fluid from silica-instilled rats also stimulates lung fibroblasts to increase collagen and noncollagen protein synthesis.

Animals↗