5-Fluorouracil treatment after irradiation impairs recovery of bone marrow functions
| Autor: | H.-P. Peterson, K. H. von Wangenheim, L. E. Feinendegen, Eugene P. Cronkite |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
Male
Pathology medicine.medical_specialty Biophysics Biology Andrology Colony-Forming Units Assay Mice Bone Marrow medicine Animals Irradiation Mitosis General Environmental Science Bone Marrow Transplantation Radiation Hematopoietic Tissue Hematopoietic Stem Cells Mice Inbred C57BL Haematopoiesis medicine.anatomical_structure Fluorouracil Mice Inbred DBA Radiation Chimera Depression Chemical Female Bone marrow Stem cell Cell Division medicine.drug |
| Zdroj: | Radiation and environmental biophysics. 26(2) |
| ISSN: | 0301-634X |
| Popis: | In mice, persisting radiation-induced growth retardation of hematopoietic tissue suggested that at least part of the surviving stem cells are genetically injured. Additional mitotic stress some time after the radiation insult might remove injured stem cells, thus improving the overall recovery of the irradiated bone marrow. Mice were treated with 5 Gy whole-body gamma irradiation. Two weeks later half of the animals were injected i.v. with 150 mg/kg 5-fluorouracil (5-FU), the other half remained untreated (5 Gy-controls). 2 or 10 weeks later, femoral cellularity and CFU-S content, proliferation ability of transplanted bone marrow and the compartment ratio (CR; ratio of splenic IUdR incorporation at day 3 and number of CFU-S transfused) were determined. Four weeks after 5 Gy and 2 weeks after 5-FU treatment all parameters showed significant impairment of recovery. 12 weeks after 5 Gy and 10 weeks after 5-FU CFU-S and CR were still reduced compared to the 5 Gy-controls. 5-FU treatment of unirradiated mice did not produce permanent effects on the quality of stem cells or the hematopoietic microenvironment. It is concluded, therefore, that an increased proliferation stimulus does not aid in the removal of injured CFU-S and may even impair recovery of bone marrow functions by increasing the proportion of genetically injured stem cells which continue proliferation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink