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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accumulation of lipids, including phospholipids, in lungs was accompanied by a proliferative-cellular reaction. The proliferation of cells was caused by accumulation of lipids. One of possible mechanisms of interrelation between lipids and collagen synthesis was as follows: in silicosis degradation of macrophages was accompanied by secretion into the medium of phospholipids, which inhibited free radical oxidation; in this case the decreased formation of cytotoxic products caused the cell proliferation, including fibroblasts, which produced collagen. The importance of lipids in collagen formation was corroborated: by accumulation of lipids, which preceded the hydroxyproline increase (scleroproteins, collagen), by development of the proliferative-cellular reaction together with the higher phospholipid-hydroxyproline level as compared with control, by formation of earlier sclerosis of silicotic nodes in "condensed" silicosis with the simultaneous increase in absolute content of phospholipids and total lipids. This role of lipids was also supported by the observed correlation between the absolute contents of scleroproteins and lipids within all steps of "quartz" silicosis development.
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PMID:[Interrelationships between lipids and scleroproteins in silicosis caused by crystalline and condensed modifications of silicon]. 20 1

Although the pulmonary and extrapulmonary manifestations of silicosis in humans have been extensively documented, the mechanisms by which the fibrogenic effects of silica are manifested remain obscure. In this review, both in vitro and in vivo models of silicosis are discussed, with emphasis on the potential methodological pitfalls of each. In animal models, for example, species variability, silica type and route of administration all effect the results obtained. Tissue culture work has provided evidence that the fibroblast-macrophage interaction is a key event in fibrogenesis. However, critical variables in experimental design make it difficult to compare the often conflicting results of different workers. Experimental conditions that directly affect collagen chain biosynthesis and subsequent hydroxylation of proline appear to be of particular importance. It is concluded that, in part because of methodological difficulties, there are insufficient data to draw firm conclusions regarding the effect of silica-exposed macrophages on collagen biosynthesis by fibroblasts in vitro; there are few, if any, data concerning the role of the macrophage that has ingested silica in human or animal models of silicosis.
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PMID:Silicosis and fibrogenesis: fact and artifact. 22 87

A group of 200 g male Sprague-Dawley rats was injected with 75 mg of quartz (less than 5 mu particle size) and changes in lung DNA, noncollagenous protein, total lipids, and collagen were studied after 6, 24, 72, 96, and 144 hr. Another group of rats received 10, 30, 59, and 75 mg quartz and the above lung analysis was performed 6 days later. Control rats received saline only. Both sets of experiments indicate that striking changes in the above parameters occur very early. The sequence of statistically significant changes was: lung weight (24 hr), DNA (24 hr), noncollagenous proteins (72 hr), total lipids (72 hr), collagen (144 hr). At the dose of 30 mg quartz/lung all the above parameters were significantly increased within 6 days after the lung injury. It is proposed that in early stages of experimental silicosis an excessive amount of collagen accumulates in the lung. Later, some of the deposited collagen is resorbed. This indicates that in the course of the silicotic fibroproliferative inflammation, the balance between collagen deposition and degradation varies.
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PMID:Early changes in the chemical composition of the rat lung after silica administration. 22 75

Granulomatous lesions of the lungs and regional bronchopulmonary lymph nodes in laboratory animals which developed spontaneously but were of epidemic nature are described. Stages of the development of pulmonary lymphoepithelioid granulomas and giant cells, the appearance of caseose-like necrosis, and the development of sclerosis of the nodules are observed. The features of sclerosing of the nodules, localization of histiocytes, macrophages, and collagen fibers are similar to those in a silicotic process in the lungs developing upon administration of Si. Micelium of Aspergilli fungus detected in a number of cases is likely to be the cause of the lesion. The nodular process in its early phases can be differentiated from tuberculosis, pseudotuberculosis, sarcoidosis, and in late stages from nodular silicosis and other granulomatous reactions of hypersensitivity of the delayed type.
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PMID:[Granulomatous lesions in the lungs of experimental animals]. 68 98

Methods of scanning, transmission electron microscopy and cytochemistry were applied to the study of the development of experimental silicosis against the background of polyvinylpyridine-N-oxide administration. The majority of the macrophages retained their functional activity and realized quartz phagocytosis, eliminating it through the airway. Bringing the proteins on the cell surface in the fibroblasts was delayed, and formation of collagen fibers decreased. Application of the polymere prevented development of fibrosis of the lungs.
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PMID:[Cytopharmacologic effect of using polyvinylpyridine-N-oxide in experimental silicosis]. 85 57

The successive differentiation in the series lymphocyte--(lymphocyte-type cell--precursor)--weakly differentiated cell (polyblast)--profibroblast--fibroblast was shown by means of scanning and transmission electron microscopy. In the focus of aseptic inflammation and in the zones of pneumosclerosis (silicosis), the ultrastructural and cytochemical cell rearrangement took place which was accompanied by the development of protein synthesizing organelles and the formation of folded surface. The collagen fibers run from the surface of the differentiated fibroblasts in the ground substance and preserve the direction of their growth with respect to the spatial position of cells.
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PMID:[Fibroblast differentiation during collagen formation]. 90 51

Content of hydroxyproline, thyrosine, hexuronic acids, hexoses and dry weight of lungs were studied in animals with pneumoconiosis, caused by various agents: two types of silicosis, induced by crystalline and condensed modifications of silica, and anthracosis, caused by anthracite. The data obtained showed that in all the types of pneumoconiosis dry weight of defatted lungs was increased with simultaneous increase of hydroxyproline content in the tissue. The more pronounced alterations were observed in silicosis. In all the types of pneumoconiosis within the experimental period content of hexuronic acids was higher in impaired animals as compared with control ones; the increase in content of hexuronic acids preceded the accumulation of hydroxyproline. Content of hexoses and thyrosine was distinctly increased within 2 days, which apparently correlated with the processes of exudation. Then it was decreased and at the later steps of the impairment amount of hexoses and thyrosine was shown to increase with simultaneous accumulation of hydroxyproline. Dynamics of accumulation of non-collagen components of connective tissue in lungs depended upon the type of a dust to which the animals were exposed.
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PMID:[Content of hexuronic acids, hexoses and tyrosine in the lung tissue in experimental pneumoconiosis]. 102 91

In order to study the progress of pulmonary silicosis in rats of different ages, intratracheal injections of (50 mg/150 g body weight) quartz dust of particle size less than 5 mu were given as a single dose and studies were made over a period of 180 days. The pulmonary macrophage reaction and phagocytosis in the younger age group of rats was different from that in the older animals at 30 days postinoculation. The formation of silicotic nodules was delayed in the younger animals. They consisted of thick reticulin fibers and some collagen fibers; in the older group of rats large silicotic nodules with dense collagination developed towards the termination of the experiment (180 days). The present results indicate a possible direct relationship between age and the development of experimental pulmonary silicosis in rats.
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PMID:A study of the age factor in experimental silicosis in rats. 114 25

Scleroderma-like diseases can be induced by a number of chemical compounds, such as plastics, solvents and drugs. Contaminated rapeseed oil was the cause of the toxic oil syndrome and L-tryptophan induces the so-called eosinophilia-myalgia-syndrome. On the other hand, paraffin and silicon can trigger so-called adjuvant disease, while long-term exposure to silica can lead to idiopathic scleroderma (associated with silicosis in some cases). In addition to the clinical features, some pathogenetic data in the literature, such as genetic factors (HLA, chromosomal anomalies, enzyme deficiencies) and the metabolism of chlorinated ethylenes via reactive epoxide intermediate products, and our own findings are reported. Silica-induced scleroderma cannot be distinguished from the idiopathic form by epidemiological, clinical or immunological studies or by parameters referring to the blood vessels or collagen metabolism. In cell culture studies it has been shown that macrophages/monocytes release IL1, IL6 and TNF after ingestion of silica, which affects fibroblasts, T-helper cells and endothelial cells. Comparative results from the silicosis literature are reported. Finally, the possibly stimulating role of ionizing irradiation (uranium mining) in favouring the development of scleroderma is discussed.
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PMID:[Chemically-induced scleroderma]. 150 11

The inhalation toxicity of three amorphous silicas (Aerosil 200, Aerosil R 974 and Sipernat 22S) was compared with that of quartz dust. Rats were exposed to 1, 6 or 30 mg Aerosil 200/m3, 30 mg Aerosil R 974/m3, 30 mg Sipernat 22S/m3 or 60 mg quartz/m3 for 6 hr/day, 5 days/wk for 13 wk. Some rats were killed at the end of the exposure period and some were killed 13, 26, 39 or 52 wk after the end of exposure. Clinical signs, body weight, haematology, biochemistry, urinalyses, organ weights, retention of test material in the lungs and regional lymph nodes, collagen content of the lungs, and gross and microscopic pathology were determined in order to disclose possible adverse effects and to study the reversibility, stability or progression of the effects. All test materials induced increases in lung weight, and pulmonary lesions such as accumulation of alveolar macrophages, inflammation, alveolar bronchiolization and fibrosis. In addition, rats exposed to Aerosil 200, Aerosil R 974 or quartz developed granulomatous lesions. Silicosis was observed only in quartz-exposed animals. At the end of the exposure period, Aerosil 200 and quartz had induced the most severe changes. Quartz dust was hardly cleared from the lungs and the changes in the lungs progressed during the post-treatment period, and eventually resulted in lesions resembling silicotic nodules and in one squamous cell carcinoma. Although Aerosil 200 was very quickly cleared from the lungs and regional lymph nodes, the changes in these organs were only partly reversed during the post-exposure period in rats exposed to 30 mg/m3. Aerosil R 974 and the lower levels of Aerosil 200 resulted in less severe, and mostly reversible, changes. The slightest changes were found after exposure to Sipernat 22S, notwithstanding the persistence of this silica in the lungs during the major part of the post-treatment period. The results of this study revealed that only quartz induced progressive lesions in the lungs resembling silicotic nodules. Of the amorphous silicas examined Aerosil 200 induced the most severe changes in the lungs, which only partly recovered, whereas Sipernat 22S induced the least severe, completely reversible lung changes.
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PMID:Subchronic inhalation toxicity of amorphous silicas and quartz dust in rats. 164 30


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