Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation.
- Author:
Hae June LEE
1
;
Joong Sun KIM
;
Myoung Sub SONG
;
Heung Sik SEO
;
Miyoung YANG
;
Jong Choon KIM
;
Sung Kee JO
;
Taekyun SHIN
;
Changjong MOON
;
Sung Ho KIM
Author Information
- Publication Type:Brief Communication ; Research Support, Non-U.S. Gov't
- Keywords: acute radiation syndrome; amifostine; hippocampus; memory impairment; neurogenesis
- MeSH: 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
- From:Journal of Veterinary Science 2010;11(1):81-83
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
