The effect of bleeding on spleen colony-forming units (CFU-S) and on in vitro colony-forming cells with colony-stimulating factor (CFU-C) and erythropoietin (CFU-E) has been evaluated. The in vivo and in vitro colony-forming cells of the bone marrow show a decrease which for the CFU-E, CFU-C follows a shortlived increase. In the spleen, all progenitor cells assayed have shown a significant and sustained increase

No abstract

The effect of some cycle-dependent anticancer drugs on CFUs has been studied in transfused polycythemic mice. In untreated animals during passive plethora erythropoiesis is depressed but the content of CFUs per femur remains constant. In treated plethoric mice the femural content of CFUs is similar or higher than that found in treated controls after administration of adriamycin, vinblastine, cyclophosphamide, it is lower when the mice receive azathioprine or hydroxyurea. These results suggest that suppression of erythropoiesis does not uniformly affect the susceptibility of pluripotent stem cells to anticancer drugs. Interpretation of the reported findings is difficult as it must take into account a complex interplay of a number of factors.

The possible protective action of sodium-2-mercaptoethanesulfonate (mesna) on hemotoxicity induced by anticancer drugs was tested in normal mice. Mesna (100 mg/kg b.w.) was injected i.v. 1 h before the i.v. administration of cyclophosphamide (10, 120, and 200 mg/kg b.w.), doxorubicin (4.32, 7.2, and 12 mg/kg b.w.) and cis-diamminedichloroplatinum (5.4, 9, and 15 mg/kg b.w.). Results show that in this experimental model mesna does not seem to protect against toxicity of the tested anticancer drug on hemopoietic progenitor cells.

The changes in the blood toxicity of some antitumoral chemotherapeutic agents in the presence of erythropoiesis activation by bleeding are evaluated. The general toxicity seems to be unaffected but the damage to erythropoiesis proved, in absolute terms, to be more severe in the bled animals. The recovery of hematopoiesis was slower after some drug than others. These results are discussed in the light of present knowledge of hematopoietic kinetics and of the relationships between antiblastic drugs and staminal hematopoietic compartments.