Only does transfusion of GT3-mobilized progenitors inhibit translocation but this treatment also reduces polymicrobial infections, particularly by Gram-negative species. These findings are consistent with older reports demonstrating the effect of a-tocopherol in attenuating the incidence of bacterial translocation in rats. We recently have reported that tocopherol succinate, tocopherol-succinatemobilized progenitors, and myeloid progenitor treatment inhibit bacterial translocation in 6 ˚Co c-irradiated CD2F1 mice. These results support our current findings regarding GT3-mobilized progenitors. Additionally, we have observed high levels of endotoxin in vehicle-mobilized progenitor recipients. It is important to note that endotoxin is associated with mice infected with Gramnegative bacteria only. Thus, the numbers of mice with high levels of endotoxin do not reflect the total number of mice, which develop bacterial infection. Jejunum histopathology demonstrated that transfusion of GT3-mobilized progenitors into irradiated mice mitigates radiation-induced GI injury. There was significant recovery in GT3-mobilized progenitor recipients compared to untreated control and PKH26-labelled mobilized cells were detected by fluorescence microscopy in various organs of recipient mice. Similar recovery of radiation-induced GI injury was observed earlier with tocopherol succinate. There are a number of major advantages observed in the mouse model described here that make GT3-mobilized progenitors attractive for the treatment of patients/casualties with ARS: a) GT3-mobilized progenitor therapy is essentially non-toxic, b) GT3-mobilized progenitor therapy clearly allows for a broader treatment range for treating both the hematopoietic and gastrointestinal-related subsyndromes of ARS, c) GT3 is stable at room temperature and suitable for long-term storage, d) GT3 may replace currently used G-CSF for progenitor mobilization in the clinic, and e) GT3 can be administered via a FDA-approved vehicle. In comparison, G-CSF is requires continuous cold storage, making its MK-4827 msds availability difficult during any disaster scenario. These characteristics make GT3-mobilized progenitors a suitable candidate as a bridging therapy for acute radiation victims that can be administered in the field with minimal infrastructure requirements. With further preclinical development in large animals and clinical trials in future, we may be able to provide an appropriate protocol for the clinical management of individuals suffering from high doses of ionizing radiation. In summary, GT3 has been shown to be attractive and promising radiation countermeasure using mouse and nonhuman primates models. It induces high levels of G-CSF in circulation within 24 h of sc administration that leads to mobilization of marrow progenitors into peripheral blood. This study suggests that mobilized progenitors mitigate radiation injury in irradiated mice. Efficacy of such cells can be abrogated by administering a G-CSF antibody to donors, suggesting that mobilization of progenitors by GT3 is a G-CSF-dependent phenomenon.