Chinese hamster ovary (CHO) cells, synchronized by selecting mitotic cells, received 300 rads of X-radiation at various intervals during the cell-cycle and were examined for cell number until they had completed their next wave of division . These growth curves were analysed for division delay in relation to type of media, i .e . modified Ham's F-10 or modified McCoy's 5 a, and to culturing conditions, i .e . monolayer or suspension . Regardless of the type of media or culturing conditions used, mitotic cells were delayed somewhat longer (0 . 55 min/rad) than early-mid G, cells, and then the delay increased with cell age from early-mid G, (0 . 32 min/rad) to late S-early G 2 (0 . 84 min/rad) . Thus, radiosensitivity during the cell-cycle approaches in late S phase a maximum for division delay in contrast to a minimum for cell killing and chromosomal aberrations. Furthermore, division delay was not increased by either incorporating bromodeoxyuridine into the DNA or treating the cells with hypertonic medium,' although each of these treatments increased mortality and chromosomal aberrations by factors of 1 .45-2 . 0 . All this evidence suggests that the site of action involved in X-ray-induced division delay differs from that involved in chromosomal aberrations and cell killing .