Respirable quartz and kaolin induction of apoptosis in rat pulmonary macrophage NR8383 cells.
Gao-N; Keane-M; Ong-T; Wallace-WE
Environ Mol Mutagen 2000 Jan; 35(Suppl 31):25
Respirable-sized quartz and kaolin dusts were tested for their induction of apoptosis in the rat pulmonary macrophage NR 8383 cell line. The effects of dust pre-incubation with the dipalmitoylphosphatidylcholine (DPPC) component of pulmonary surfactant on the induction of apoptosis were measured. Occupational exposure to respirable silica quartz dust can result in an acute inflammatory response followed by chronic fibrotic change in the lungs. Kaolin aluminosilicate dust generally is not associated with significant fibrotic lung disease. Pretreatment of dust particles with DPPC is known to suppress some otherwise prompt in vitro cytotoxic activities of quartz and kaolin. Apoptosis was measured by two assays: a propidium iodide staining procedure for DNA ploidy analysis using flow cytometry; and an ELISA assay for mono- and oligonucleosomes. Cells challenged in vitro for 6 hours by untreated quartz dust showed a dosedependent increase in apoptosis as indicated by both flow cytometry and ELISA assays. Kaolin was less strongly active than quartz in the ELISA assay and kaolin was active only at high concentrations in the flow cytometry assay. Cells also were challenged over a one- to five-day period by quartz or kaolin at a single concentration. DPPC pretreatment of both dusts delayed their induction of apoptosis as measured by the ELISA assay; partial activity was restored at 3 and 5 days after challenge. Neither DPPC-treated dust showed significant activity in the flow cytometry assay.
Quartz-dust; Respirable-dust; Laboratory-animals; Animals; Animal-studies; Dusts; Dust-particles; Particulates; Particulate-dust; Occupational-exposure; Pulmonary-system-disorders; Respiratory-system-disorders; Silica-dusts; Silicates; Lung-disease; In-vitro-studies
Environmental and Molecular Mutagenesis