Abstract
Low dose (80 .mu.g/kg) of [the antineoplastic drug] actinomycin D (AD) produced a significant but transient inhibition of hemopoietic stem cell (CFU) proliferation in chimeras or in mice regenerating after sublethal irradiation. The same dose of AD had no effect on the resting CFU population. During the proliferation inhibition period, CFU proved to be insensitive to the killing effect of [3H]thymidine in vitro and hydroxyurea (HU) in vivo. In Ehrlich ascites tumor bearing mice CFU turnover rate was enhanced. Eighty .mu.g/kg AD produced a selective effect in these mice: it protected the proliferating CFU population without diminishing the effect of hydroxyurea on tumor cells.