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.

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.

Study of inflammatory responses to crocidolite and basalt wool in the rat lung.

The subacute effects of crocidolite and basalt wool dusts were studied by nmeans of biochemical, morphological. and histological methods 1 and .3 mo after intrabronchial instillation.

Effects of sodium diethyldithiocarbamate on type II pulmonary epithelial cells in vitro.

Dithiocarbamates (DDTC) are chemicals widely used in the form of pesticides, therapeutic and chelating agents, and scavengers. Since DDTC interfere with SH, Cu, and Zn enzymes due to chelating properties, it was of interest to clarify, in primary culture of type II alveolar pneumocytes, the effect of this compound upon enzymes of glutathione cycle, Cu, Zn-superoxide dismutase, and the membrane structure of cells. DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found.

Characterisation of lectin binding patterns of mouse bronchiolar and rat alveolar epithelial cells in culture.

Lung epithelial cell differentiation pathways remain unclear. This is due in part to the plasticity of these cells and the lack of markers which accurately reflect their differentiation status. The aim of this study was to determine if lectin binding properties are useful determinants of functional differentiation status in vitro.

In vitro and in vivo tests for determination of the pathogenicity of quartz, diatomaceous earth, mordenite and clinoptilolite.

The effects of samples of crystalline quartz, diatomaceous earth, mordenite and clinoptilolite were investigated in vitro (as concerns erythrocyte haemolysis and lactate dehydrogenase (LDH) release from peritoneal macrophages) and in vivo (on LDH, protein and phospholipids in rat bronchoalveolar lavage (BAL), and phospholipids in rat lung tissue). The respirable mineral samples were instilled intratracheally. Determinations in the BAL were carried out after 15, 60 and 180 days, and in the lung tissue after 90, 180 and 360 days.

Surface changes in type II pneumocytes isolated from rats during the cultivation.

Type II cells isolated from the rat lung were maintained in culture for 8 days. The activity of alkaline phosphatase and lectin binding properties were studied. The alkaline phosphatase activity and the number of lamellar bodies were continually decreasing during the studied time period.

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.

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.

A study on lung toxicity of respirable hard metal dusts in rats.

The aetiology of hard metal lung disease has not been clarified so far. The pulmonary toxicity of respirable dusts collected in a hard metal factory was studied in vivo in rats. The effect of the samples was examined 1, 4, 7 and 30 days after single intratracheal injection.

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 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 pulmonary toxicity of cinnamon dust in rats.

The histopathological effect of a single intratracheal dose of respirable cinnamon dust, cinnamon dust extract, and cellulose dust on the lungs of rats was studied sequentially one, seven days and one month after treatment. Exposure to respirable cinnamon and cellulose dusts resulted in alveobronchiolitis at the end of the first and seventh day, and fibrotic changes by the end of the first month. As the extract of cinnamon dust caused no histopathological alterations, it is assumed that the cellulose content of cinnamon dust was responsible for the histological reactions.

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.

On the structural differences in the membranes between ciliated bronchial and non-ciliated lymphoepithelium in rats.

The membrane structure of bronchial ciliated epithelium and lymphoepithelium was studied in rats by lectin histochemistry. The lymphoepithelium, contrary to bronchial ciliated epithelium, did not contain terminal beta-D-galactose residues. Moreover L-fucose and beta-D-Gal (1-3)-D-GalNAc residues, being masked, could be visualized only after enzymatic digestion of terminal sialic acid.

Studies on the cytotoxicity of ceramic respirable dusts using in vitro and in vivo test systems.

The effect of a number of ceramic raw materials and airborne samples in workplaces has been investigated in vitro [erythrocyte haemolysis, macrophage TTC (2,3,5-triphenyl-tetrazolium chloride) reduction and LDH (lactate dehydrogenase) activity] and in vivo (protein, LDH and phospholipid in cell-free bronchopulmonary lavage). In the in vitro experiments described we were able to distinguish between the dusts causing different types of reaction in the lung. Dusts classified as 'quartz type' in vitro were also cytotoxic in vivo.

Biological effects of the respirable dusts from ore mines.

The biological effects of ore dusts were examined on peritoneal macrophages in vitro and on rat lung in vivo. The methylene blue adsorption of the dust samples, cytotoxicity, and phospholipid and hydroxyproline content of the lung were determined. It was realized that the examined ore samples had cytotoxic effects and from the in vitro results one can get information about the type of damage to be expected in the lung tissue.

Occupational exposure to organophosphorus insecticides and synthetic pyrethroid.

Dermal and respiratory exposure to pirimiphosmethyl, dimethoate and permethrin were determined for applicators and operators in greenhouse tomato spraying operations. Dermal exposure is several times higher than the degree of respiratory exposure. Dermal exposure in terms of different parts of the body shows significant differences.

Short term in vivo method for prediction of the fibrogenic effect of different mineral dusts.

The effect of intratracheal introduction of different metal and mineral dusts and the change in activity of pulmonary acidic phosphatase have been studied as a function of time (72 h, 2 weeks, 1, 12, 20 months). The activity and localization of acid phosphatase were compared with the degree of pulmonary damage caused by dusts. The degree of fibrosis was determined on the basis of the composition of cells and fibres, according to Belt and King's classification.

Experimental pneumoconiosis due to dusts of ore mines. II.

The effect of dead rock dusts from a Hungarian ore mine was studied in long term experiments. Histological changes caused by intratracheally introduced respirable mixed rock patterns (Porphyry, Enargite, Scarnic grained- and drill-cuttings) were examined and compared with standard DQ12 quartz samples 3, 6, 12 and 20 months after treatment. All three dusts proved to be fibrogenic, although in different extent.

Comparative histopathological and biochemical analysis of early stages of exposure to non-silicogenic aluminium silicate- and strongly silicogenic quartz-dust in rats.

One group of male CFY rats was given bentonite with high aluminium silicate content, the other group was given quartz dust, intratracheally. It has been stated that between 12-72 hours after the dust-exposure, the histological reactions developing upon the effect of non-silicogenic bentonite and silicogenic quartz are identical. Similarly in both groups lipid and phospholipid content of the lung shows a slight increase; the composition of phospholipids does not alter due to the effect of the two dusts.

Experimental pneumoconiosis due to dusts of ore mines, I.

Male CFY rats were injected into their trachea with a suspension of dust of ore mine dead rock of high quartz content and mixed composition (particle size: 0-60 micrometers). Three and six months after treatment, foreign body granulation and after twelve months a non-fibrotic diffuse lung disease was seen in the animals. After twelve months of exposure, non-specific, mature sinus histiocytosis and small focal epitheloid cell reaction were found to develop in the cervical, lung-hilar and retroperitoneal lymph nodes.