In vitro cytotoxic effects of wollastonites on rat hepatocytes: II. Lipid peroxidation and glutathione depletion.
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Biomedical subjects
Publications and source records attributed to Q Rahman.
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In the present study, cytogenetic effects of Indian chrysotile asbestos in rat bone marrow cells after 290 days of intratracheal inoculation (5 mg dust/0.5 ml normal saline), when it develops massive pulmonary fibrosis, were investigated. The pulmonary fibrosis was confirmed by both histopathological studies and increased collagen content in the lung of the treated animals. In the asbestotic rats a significant increase in chromosomal aberrations was recorded and a decrease in mitotic index of bone marrow cells. The types of chromosomal aberrations in these cells were chromatid gaps and breaks. The results indicate the significant cytogenetic changes in the bone marrow cells of asbestotic rats and also suggest that these changes directly or indirectly may be one of the biological events involved in eliciting the asbestos-mediated toxic responses.
In order to determine the pulmonary toxicity of kerosene and its ignition product (soot) in asbestos exposed subjects, the activities of phase I and phase II drug metabolizing enzymes in rat lungs after single intratracheal co-exposure to Indian chrysotile asbestos and kerosene or its soot and Indian chrysotile were assayed. Exposure to kerosene or its soot resulted in a significant increase in the level of microsomal cytochrome P-450 and the activity of P-450 dependent monooxygenase, benzo(a)pyrene hydroxylase, as well as in the activities of microsomal epoxide hydrase and cytosolic glutathione-S-transferase (GST). However, in chrysotile exposed animals a reverse pattern in these parameters was recorded. The co-exposure to chrysotile and kerosene or chrysotile and soot led to a significant depletion in cytochrome P-450 level and a decrease in the activities of benzo(a)pyrene hydroxylase, epoxide hydrase and GST when compared to kerosene and soot controls, respectively. These results suggest that asbestos by altering the pulmonary drug metabolizing enzyme system may increase the toxic potential of kerosene and its ignition product in the respiratory system.
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Hemolysis induced by native kaolin dust was found to run parallel to the amount of silicic acid dissolved from it. Native mica and talc dusts were hemolytic only to a small extent and the silicic acid dissolution from these dusts was also smaller in comparison to that of native kaolin. The proportionality between hemolysis and the amount of dissolved silicic acid was not consistently observed in the case of acid, alkali and water treated kaolin, mica and talc dusts.
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The dissolution of silica from amosite dust in human serum and in Ringer buffer at 37 degrees C was found to be significantly higher than that from quartz. The significance of this finding in relation to their fibrogenic effects has been discussed.
The contents of collagen, hexosamine, phospholipids, and cholesterol and the activities of acid and alkaline phosphatases, glutamic oxalo-acetate transaminase, glutamic pyruvate transminase, aldolase, hexokinase, and lactic dehydrogenase were determined in the lungs of rats 150 days after the intratracheal injection of amosite, anthophyllite, and chyrsotile. Anthophyllite did not cause any significant change, while amosite and chrysotile caused significant increases in the contents of collagen and mucopolysaccharides. Lactic dehydrogenase and acid phosphatase activities were increased by all the dusts, while the othe enzymes were not seriously affected. The biochemical significance of the findings in relation to abestosis was discussed.
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