The haemopoietic stem cells forming spleen colonies (CFU-S) had on average 30 to 40% of cells engaged in the DNA synthesis in normal mice continuously over 4 years. A majority of experiments aimed at the suppression of the CFU-S proliferation, which included suppression of the T-lymphocytes by means of cyclosporin A or by adult thymectomy, administration of antibacterial and antifungal agents and maintainance of mice in a sterile environment, suppression of antibody-producing cells by a successive administration of the bacterial lipopolysaccharide and cyclophosphamide and attempts to increase the total number of CFU-S in the body through massive transfusions of bone marrow cells or by grafting plugs of the bone marrow under the kidney capsulae, have not been sufficiently effective. A transient suppression of CFU-S proliferation occurred during recovery of the haemopoietic tissue from damage caused by cyclophosphamide. The results support the view that changes in CFU-S numbers and in the proportion of them in DNA synthesis may be positively correlated when CFU-S numbers fluctuate physiologically about their normal values. The failure to manipulate the CFU-S proliferation rate easily suggests that proliferation of these cells may not be under a strong 'switch onswitch off' control.We have reported that haemopoietic stem cells, detected by the spleen colony-forming technique (CFU-S), vary considerably in their sensitivity to the lethal action of [3H]-thymidine or hydroxyurea when individual, normal mice were examined (NeEas & Znojil, 1987). The mean value of the proportion of DNA synthesizing CFU-S was about 30% in our normal mice, which is much higher than the widely accepted value of less than 10% (Lord, 1983). This paper summarizes our attempts to suppress CFU-S cycling in normal mice, which were largely ineffective. We present these observations to demonstrate the constancy of the CFU-S high proliferation rate in our normal mice and its resistance to experimental conditions that should, according to present concepts, decrease the CFU-S Proliferation.
MATERIALS A N D M E T H O D SMice CBA/Ca mice, C57Bl/lOScSn mice, CBA/Ca x C57B1/1OScSn F1 hybrids (CBFI) and DBA 2/J x C57B1/1OScSn F1 hybrids (BDF1), all of the specific pathogen-free grade IV (according to