W Sun, R Wu and JA Last
California Regional Primate Research Center, Davis 95616-8542.

The human bronchial epithelial cell line, BEAS-2B, which was immortalized by transformation with SV40 virus, when grown biphasically between 0.1 and 1.0 ppm of ozone and liquid medium showed increased release of Cr, decreased synthesis of various macromolecules, and decreased cell viability. Cell injury was a function of the concentration of ozone to which the cells were exposed. Furthermore, in proportion to the extent of cell injury, ozone exposure also induced and/or enhanced synthesis of a 45 kD protein but not any of the well- characterized heat shock proteins, e.g., HSP 70. Actinomycin D prevented enhanced synthesis of the 45 kD protein in cells exposed to ozone, suggesting transcriptional regulation of expression of the 45 kD protein. Enhanced synthesis of the 45 kD protein was not observed in cells treated with heat, cigarette smoke condensate, hydrogen peroxide, or bleomycin. High concentrations of glutathione added to the culture medium reduced ozone toxicity and ozone-enhanced synthesis of the 45 kD protein. These results suggest that ozone injury and enhanced expression of a gene encoding a 45 kD protein of as yet unknown function are coordinated in the SV40-immortalized bronchial epithelial cells.

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