This study examined whether amifostine (WR-2721) could attenuate memory impairment and suppress hippocampal neurogenesis in adult mice with the relatively low-dose exposure of acute radiation syndrome (ARS). These were assessed using object recognition memory test, the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, and immunohistochemical markers of neurogenesis [Ki-67 and doublecortin (DCX)]. Amifostine treatment (214 mg/kg, i.p.) prior to irradiation significantly attenuated the recognition memory defect in ARS, and markedly blocked the apoptotic death and decrease of Ki-67- and DCX-positive cells in ARS. Therefore, amifostine may attenuate recognition memory defect in a relatively low-dose exposure of ARS in adult mice, possibly by inhibiting a detrimental effect of irradiation on hippocampal neurogenesis.
Acute Radiation Syndrome/drug therapy/*immunology/psychology ; Amifostine/*pharmacology/therapeutic use ; Animals ; Apoptosis/immunology ; Gamma Rays/*adverse effects ; Hippocampus/immunology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Male ; Memory/*radiation effects ; Mice ; Mice, Inbred ICR ; Neurogenesis/immunology ; Radiation-Protective Agents/*pharmacology/therapeutic use