Compound 48/80 (poly-p-methoxyphenethylmethylamine), an agent commonly used to trigger degranulation of mast cells, at concentrations of 5-20 micrograms/ml suppresses the proliferation of L1210 and Friend leukemic cells in vitro, inducing the formation of giant cells, which are polykaryons. Both the proportion of polykaryons in cultures and their size (which reflects the number of nuclei per polykaryon) increase during growth in the presence of 48/80 up to 48 hr; thereafter, the cells lose viability. A predominant number of nuclei in these polykaryons contain a 4C, or higher DNA content. The data indicate that compound 48/80 impairs the cleavage (cytokinesis) and perhaps mitotic processes. Mechanisms by which compound 48/80 induces the described effects are unknown but may be related to the polycationic nature of the polymer and its interaction with the cell membrane. Certain attributes of compound 48/80 suggest that this or similar polymers may have value as research tools for the study of regulatory mechanisms involved in cell division.

Tritium‐labelled uridine ([3H]UdR) perturbs progression of L1210 cells through the mitotic cycle. the main effect manifests as a slowdown or arrest of a portion of cells in G2 and is already observed 2 hr after addition of 0.5–5.0 μCi/ml of [3H]UdR into cultures. At 2.5–5.0 μCi/ml of [3H]UdR a slowdown of cell progression through S is also apparent. Additionally, there is an increase in the number of cells with DNA values higher than 4C in cultures growing in the presence of [3H]UdR for 8–24 hr. A pulse of [3H]UdR of 2 hr duration labels predominantly (95%) cellular RNA. the first cell‐cycle effects (G2 slowdown) are observed when the amount of the incorporated [3H]UdR is such that, on average there are fewer than thirty‐six [3H] decays per cell which corresponds to approximately 12–19 rads of radiation. the S‐phase slowdown is seen at a dose of incorporated [3H]UdR twice as high as that inducing G2 effects. the specific localization of [3H]UdR in nucleoli, peripheral nucleoplasm and in cytoplasm, as well as differences in the kinetics of the incorporation in relation to phases of the cell cycle are discussed in the light of the differences between the effects of [3H]UdR and [3H]thymidine. Mathematical modelling of the cell‐cycle effects of [3H]UdR is provided.