OBJECTIVETo explore the differences of the silica-induced inhibition on cellular proliferation and hprt gene mutagenesis between lung fibroblasts and alveolar type II cells.

METHODSThe proliferation inhibitive cytotoxicity was detected by MTT (3-[4,5-Dimethylthiazolzyl]-2,5-Diphenyl Tetrazolium Bromide) colorimetric method. Mutation in the hprt gene was screened by culture in the presence of the toxic purine analog, 6-thioguanine (6-TG).

RESULTSUnder the same circumstances of silica exposure, alveolar type II cells was more sensitive than lung fibroblasts for proliferation inhibition. The median proliferation inhibition concentration (IC50) of silica on epithelial was 140 micrograms/cm2, whereas IC50 of silica on fibroblasts was 282 micrograms/cm2. At the same doses of silica, the hprt gene mutation frequency in type II cells (84.2 x 10(-6))-156.6 x 10(-6) was statistically higher than that in fibroblasts (67.6 x 10(-6)-114.3 x 10(-6), P < 0.05).

CONCLUSIONThere were significant differences of both silica-induced cell proliferation inhibition and hprt gene mutation between rat lung fibroblasts and type II epithelial cells. In vitro, cultured rat alveolar type II cells were more sensitive in cytotoxicity and hprt gene mutagenesis to silica dust than lung fibroblasts were.

Animals ; Cell Proliferation ; drug effects ; Epithelial Cells ; drug effects ; Fibroblasts ; drug effects ; Hypoxanthine Phosphoribosyltransferase ; genetics ; Lung ; cytology ; drug effects ; metabolism ; Mutation ; Pulmonary Alveoli ; cytology ; drug effects ; Rats ; Silicon Dioxide ; toxicity