The cellular basis of long-term marrow injury after irradiation.
Haemopoietic recovery from radiation injury can appear complete when measured by blood cell counts, but this can hide deficiencies in the precursor cell populations because of compensatory mechanisms of increased numbers of divisions in the maturing cell populations and increased cycling of the stem cells. These mechanisms can operate for quite long but finite periods, before they fail which then leads to hypoplasia. Also, while these mechanisms are operating, small further injuries could precipitate marrow failure. Persistent injury in the stem cell population can be induced by quite small doses, and in mice the threshold total dose is probably in the region of 1.5 Gy using fractionated whole-body irradiations. The sensitivity of the environment varies enormously, depending largely on the proliferative stress applied to the cell populations involved in the particular assay technique used. When similar tests of reproductive integrity are applied, stromal progenitor cells are more radioresistant than haemopoietic stem cells. The contribution of environmental injuries to haemopoietic defects is uncertain and difficult to assess.
D000818:Animals; D001772:Blood Cell Count; D004307:Dose-Response Relationship, Radiation; D004735:Energy Transfer; D006412:Hematopoietic Stem Cells / Q000528:radiation effects*; D006801:Humans; D051379:Mice; D011829:Radiation Dosage; D011832:Radiation Injuries / Q000473:pathology*; D011833:Radiation Injuries, Experimental / Q000473:pathology*; D011836:Radiation Tolerance; D013997:Time Factors