Abstract
Effects of 2''-chlorothymidine (2''-Cl-TdR) and its mother compound, thymidine (TdR), on cell killing induced by X and UV-irradiation have been investigated. Chinse hamster V-79 (TK+) cells as well as thymidine kinase deficient (TK-) variant cells, which were isolated from parental V-79 cells following stepwise treatment with BUdR, were incubated in a medium containing 2''-Cl-TdR and TdR after X and UV-irradiation. In the TK+ cells, both 2''-Cl-TdR and TdR enhanced the killing efficiency of X-rays and ultraviolet light. On the other hand, in the TK- cells, only 2''-Cl-TdR enhanced the killing efficiency of X and UV-irradiation, and no effect of TdR was observed. These results suggest that phosphorylation of TdR by the enzyme is essential for its ability to modify radiation response, while the enhancement of cell killing by 2''-Cl-TdR must be explained by a mechanism at least partly independent of phosphorylation.
