Abstract
Ionizing radiation (IR) is known not only to cause acute bone marrow (BM) suppression but also to lead to long-term residual hematopoietic injury. These effects have been attributed to IR inducing the generation of reactive oxygen species (ROS) in hematopoietic cells. In this study, we examined if isorhapontigenin and heyneanol-A, two analogues of resveratrol, could mitigate IR-induced BM suppression. The results of cell viability assays, clonogenic assays, and competitive repopulation assays revealed that treatment with these compounds could protect mice BM mononuclear cells (BMMNC), hematopoietic progenitor cells, and hematopoietic stem cells from IR-induced BM suppression. Moreover, the expression of genes related to the endogenous cellular antioxidant system in hematopoietic cells was analyzed. The expression and activity of SOD2 and GPX1 were found to be decreased in irradiated BMMNC, and the application of the resveratrol analogues could ameliorate this damage. Our results suggest that in comparison with resveratrol and isorhapontigenin, treatment with heyneanol-A can protect hematopoietic cells from IR-induced damage to a greater degree; the protective effects of these compounds are probably the result of their antioxidant properties.
Highlights
Radiation therapy is a common and effective tool in the management of a wide variety of tumors; in some cases, it may be the single best treatment for cancer
Several studies have demonstrated that the induction of oxidative stress in hematopoietic cells is associated with sustained oxidative DNA damage; this results in a persistent loss of proliferative capacity in hematopoietic progenitor cells (HPCs) and hematopoietic stem cells (HSCs) [4, 6, 7]
We examined whether the REV oligomers ISOR and HEY-A could inhibit ionizing radiation (IR)-induced Bone marrow (BM) injury in mice
Summary
Radiation therapy is a common and effective tool in the management of a wide variety of tumors; in some cases, it may be the single best treatment for cancer. Bone marrow (BM) suppression is the most common dose-limiting side effect during radiation therapy [1, 2]; BM suppression is the primary cause of death following accidental exposure of a patient to a high dose of total body irradiation. Injuries due to IR occur as a result of the ionization of water resulting in the formation of reactive oxygen species (ROS), notably hydroxyl radicals, increasing oxidative stress [4, 5]. Our recent studies have indicated that a persistent IR-induced increase in the production of reactive oxygen species (ROS) can be achieved in hematopoietic cells, in part, via the downregulation of superoxide dismutase (SOD) and glutathione
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