Comparison of radon‐daughter‐induced effects in repair‐proficient and repair‐deficient cho cell lines

The radiobiological effects of the radon daughter 212Bi were investigated in the Chinese hamster ovary cell line AA8 and its radiosensitive derivative EM9. EM9 cells rejoin radiation‐induced DNA strand breaks more slowly than do AA8 cells. Three endpoints were examined: cell killing, G2‐induced chromosome aberration frequency, and mutation induction at the hypoxanthine (guanine) phosphoribosyltransferase (HGPRT) locus. Cells were exposed to the alpha‐emitter 212Bi chelated to diethylenetriaminepentaacetic acid (212Bi‐DTPA). As expected, 212Bi‐DTPA was more effective than X‐rays in producing cytotoxicity, chromosome aberrations, and gene mutations. The relative biological effectiveness (RBE) for all three endpoints ranged from about 2 for chromosome aberrations to 4.4 for mutation induction. EM9 was more sensitive than AA8 cells to the cytotoxic and clastogenic effects of both X‐rays and 212Bi‐DTPA, suggesting that the repair deficiency in EM9 cells affects response to low‐and high‐linear energy transfer (LET) radiation for these endpoints. There was no significant difference between these two cell lines in their mutagenic response to X‐rays and AA8 was slightly more sensitive to the mutagenic effects of alpha radiation. These results suggest that alterations in DNA repair ability may affect response of cells to both low‐ and high‐LET radiation‐induced cytotoxicity and clastogenicity, but they appear to have little effect on gene mutation induction.