Effects of various mineral dusts on macrophages in vitro.
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Animals↗
Biomedical subjects
Z Adamis
Publications and source records attributed to Z Adamis.
In vivo pulmonary toxicity of cellulose in rats.
Cellulose after a single intratracheal dose (15 mg per animal) brought about fibrosing granulomatous alveobronchiolitis and an increase of IgA production in the bronchoalveolar lavage. Fibrosing alveolitis showed moderate progression as a function of time. With different morphological methods, injury of type I pneumocytes and the incomplete repair of type II pneumocytes were detected. The damage of the alveolar epithelium initiated and activated a series of processes that led to definite pulmonary alterations: pulmonary fibrosis leading to the disintegration of the alveolo-capillary morphological functional unit.
Animals↗
In vitro and in vivo assessment of the pulmonary toxicity of cellulose.
The lung-damaging effect of intratracheally administered cellulose was studied by biochemical and histological methods. Cell count, protein, phospholipid, lactate dehydrogenase and acid phosphatase were determined in bronchoalveolar lavage fluid 1, 3 and 7 days after intratracheal instillation. Histological tests were performed after days 1, 3 and 30. In vitro, cellulose did not damage the macrophage cells. In vivo, interstitial oedema as well as the initial signs of inflammation could be detected in the lung after the first day. Inflammation after 1 week could be noted, partly interstitial and partly intra-alveolar and intrabronchial. In the bronchoalveolar lavage fluid, protein, lactate dehydrogenase, acid phosphatase, phospholipid and cell count were enhanced after days 1 and 3. After 1 month, the developing bronchioalveolitis is fibrous in character. Contrary to the in vivo study, cellulose did not damage rat peritoneal macrophages.
Animals↗
Combined pulmonary toxicity of diethyldithiocarbamate and lead (II) oxide in rats.
The pulmonary toxicity of sodium diethyldithiocarbamate and lead(II) oxide alone or in combination was studied in rats after a single intratracheal instillation. The lead content in the lungs and the whole blood was determined and it has been found that the clearance of lead from the lung was delayed by dithiocarbamate complex formation, which probably had a role in increased IgA levels in the bronchoalveolar fluid and the induction of local immune response. The combined exposure gave rise to calcium deposits in the lungs both extra- and intracellularly after 1 month of exposure. Both separate and combined exposure invoked permanent injury in membranes or dystrophic changes in the cytoplasm of pneumocytes, which may initiate and generate a series of events leading to fibrosing alveolitis.
Adjuvants, Immunologic↗
Effects of lead(II) nitrate and a dithiocarbamate fungicide on the rat lung.
The pulmonary toxicity of two potential environmental pollutants was studied in rats 1, 7 and 30 days after a single intratracheal instillation of lead nitrate and Dithane M-45 (mancoceb), either individually or in various combinations. The cell count, protein, phospholipids and lactate dehydrogenase level were determined in the bronchoalveolar lavage fluid, as were the protein, phospholipids and acid phosphatase contents in the lung tissue. Lead nitrate and Dithane M-45 induced acute inflammation reactions with different features. The effects of mixtures of lead nitrate and Dithane M-45 were found to be different from those of the individual components.
Acid Phosphatase↗
Role of cellulose in wood dust-induced fibrosing alveo-bronchiolitis in rat.
Our experiments suggest that in the development of plant dust-induced fibrosing alveobronchiolitis--Scadding's fibrosing alveolitis--the cellulose content of plant dusts has a decisive aetiological role. Namely, the wood dust (pine) and the cellulose induced morphologically identical granulomatous inflammation and fibrosis, whereas the fibre-free extract of wood dust did not cause pathological changes in the lungs. The induction of H2O2 and superoxide anion production, shown in vitro in leucocytes, probably has an important role in the development of fibrosis.
Animals↗
Combined pulmonary toxicity of cadmium chloride and sodium diethyldithiocarbamate.
The pulmonary toxicity of sodium diethyldithiocarbamate and cadmium chloride, each separately and in combination, was compared in Sprague-Dawley rats after single intratracheal instillation in sequential experiments by chemical, immunological and morphological methods. With combined exposure, the cadmium content of the lungs increased permanently relative to that of the lungs of just cadmium-treated animals. Immunoglobulin levels of the whole blood did not change, whereas in bronchoalveolar lavage the IgA and IgG levels increased significantly. Morphological changes were characteristic of the effects of cadmium but were more extensive and more serious than in the case of cadmium administration alone: by the end of the first month, interstitial fibrosis, emphysema and injury of membranes of type I pneumocytes developed and hypertrophy and loss of microvilli in type II pneumocytes were detectable. These results showed that although dithiocarbamates as chelating agents are suitable for the removal of cadmium from organisms, they alter the redistribution of cadmium within the organism, thereby increasing the cadmium content in the lungs, and structural changes are more serious than observed upon cadmium exposure alone.
Animals↗
Comparative in vitro toxicity of cadmium and lead on redox cycling in type II pneumocytes.
Both cadmium and lead have pulmonary toxicity: cadmium can cause lung cancer, fibrosis and emphysema; lead can induce a moderate interstitial pulmonary fibrosis. Both metals give rise to depletion of glutathione and depletion of the protein-bound sulfhydryl groups, and lead to the production of reactive oxygen species. In the primary culture of type II pneumocytes, which is one of the most important cell groups from the aspect of glutathione metabolism and thus redox balance, the effect of cadmium chloride and lead nitrate upon the enzymes of the glutathione cycle, upon superoxide dismutase and upon the structure of type II pneumocytes was examined. Depending on the concentration, cadmium inhibited each of these parameters, whereas lead nitrate significantly increased the activity of glutathione reductase while inhibiting other parameters. Both metals induced damage of the membranes of type II cells, depending on the concentration, although cadmium caused significantly more damage than lead. The data obtained suggest that both substances cause an imbalance in the redox cycle and diversely affect the function and membrane structure of type II pneumocytes.
Animals↗