Response of mammalian cell lines that undergo necrosis after ionizing irradiation to DNA-incorporated tritium and iodine-125 decays: implications for models of radiation action.

摘要

Purpose: To test the validity of enzymatic DNA repair-based models of ionizing radiation-induced mammalian cell killing. Materials and methods: Sensitivity to ionizing radiation-induced killing was determined by clonogenic survival assay. Results: A panel of seven cell lines that have apparently normal enzymatic DNA repair capability and die predominantly by necrosis were shown to have marked differences in their sensitivity to killing by gamma- or X-irradiation. Despite such differences, the pseudo-diploid cell lines CHO, V79, and Vero (when corrected for differences in cell cycle distribution) and normal mouse embryo fibroblasts all had comparable D(o) values for killing by DNA-incorporated (125)I that were in the range of 57-66 decays; whilst the near-tetraploid or-triploid B16-F1, RUC-2 and SQ-20B cell lines had D(o) values of around 130 (125)I decays. The sensitivity of these cell lines to killing by DNA-incorporated (3)H decays was similarly related to ploidy. Conclusions: Differences in sensitivity to killing by DNA-incorporated (3)H or (125)I decays between the cell lines tested were primarily related to differences in ploidy and, second, to differences in cell cycle distribution or nuclear volume. The data do not support suggestions that generalized variability in an hypothetical aspect of enzymatic DNA repair can explain differences in sensitivity to killing by external-beam, low-linear energy transfer ionizing radiation.