Cell type-specific effects of asbestos on intracellular ROS levels, DNA oxidation and G1 cell cycle checkpoint.

Exposure to asbestos fibers increases the risk of development of mesotheliomas and lung carcinomas, but not fibrosarcomas. We present data suggesting that resistance of fibroblasts to asbestos-induced carcinogenesis is likely to be connected with their lower ability to generate reactive oxygen species (ROS) in response to asbestos exposure and stricter control of proliferation of cells bearing asbestos/ROS-induced injuries. In fact, chrysotile (Mg6Si4O10(OH)8) asbestos exposure (5-10 microg/cm2) increased intracellular ROS and 8-oxo-guanine contents in rat pleural mesothelial cells, but not in lung fibroblasts.

Factors secreted by peritoneal macrophages are cytotoxic for transformed rat pleural mesothelium and mesothelioma cells.

The report is devoted to the investigation of cytotoxic action of macrophages and asbestos on transformed mesothelium and mesothelioma cells, the characterization of its specificity, and the nature of the factors mediating it. The viability of different cells after asbestos exposure was studied in co-culture with macrophages. Mesothelioma cell lines obtained from tumors developed in vivo were the most sensitive to the cytotoxic action of macrophages and asbestos.