The Target for Radiation-Induced Division Delay

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Abstract
To elucidate the subcellular target responsible for radiation-induced division delay, Chinese hamster ovary (CHO) cells growing in monolayer cultures were pulse-labeled with 125IUdR [125I-iododeoxyuridine] and the cell kinetics monitored by counting the mitotic cells selected every 10 min. 125I incorporated into DNA caused a perturbation of cell progression; unlabeled G2 cells were unperturbed. As 125I-labeled cells entered the mitotic selection window, the normalized yield of mitotic cells (number of 125I-labeled mitotic cells expressed as a fraction of cells harvested from control flasks) decreased to a level inversely proportional to the incorporated 125IUdR and remained at this level for the duration (4-5 h). To evaluate the mechanism of 125I-induced division delay, 125IUdR-labeled cells were permitted to accumulate 125I decays during the S phase (by cooling the monolayer to 4.degree. for 2 h immediately after pulse labeling) or during S and G2 phases (by cooling the monolayer to 4.degree. C for 2 h, starting 2 h after the pulse label). Cells which accumulated 125I decays only during the S phase did not experience enhanced delay. The yield of mitotic cells was reduced in cells which accumulated 125I decays during S and G2. The target for radiation-induced mitotic delay apparently is not the DNA, but a cell structure which comes in contact with the DNA during G2 or early M phase.