Radiation-induced division delay of Chinese hamster ovary cells located in G2, and in G2 between the cycloheximide and X-ray transition points, was measured by the mitotic cell selection technique. The mitotic yield (number of mitotic cells after treatment expressed as a fraction of the control) decreased with increasing radiation dose (4.5 to 34 rad). However, either because some cells were not delayed or because delayed cells recovered rapidly, the mitotic yield did not fall to zero. When cycloheximide was combined with radiation to prevent repair of the radiation damage, only cells which were past the cycloheximide transition point and not delayed by the radiation were selected. The location of the transition points determined from the combined drug plus low-dose radiation (4.5 to 34 rad) experiments indicate a dose-dependent relationship, with more cells delayed as the dose was increased. In addition, the transition point for cells treated with cycloheximide plus 150 rad of X rays was closer to division than the 150 rad of X rays alone. These results are discussed in light of a recent model for radiation-induced division delay proposed by Dewey and Highfield [Radiat. Res. 65, 511-528 (1976)].

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