Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation.
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.
Lee
Hae-June
HJ
Korea Institute of Radiological and Medical Science, Seoul, Korea.
Kim
Joong-Sun
JS
Song
Myoung-Sub
MS
Seo
Heung-Sik
HS
Yang
Miyoung
M
Kim
Jong Choon
JC
Jo
Sung-Kee
SK
Shin
Taekyun
T
Moon
Changjong
C
Kim
Sung-Ho
SH
D054508:Acute Radiation Syndrome / Q000188:drug therapy / Q000276:immunology* / Q000523:psychology; D004999:Amifostine / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000276:immunology; D000089662:Doublecortin Protein; D005720:Gamma Rays / Q000009:adverse effects*; D006624:Hippocampus / Q000276:immunology; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D008568:Memory / Q000528:radiation effects*; D051379:Mice; D008813:Mice, Inbred ICR; D055495:Neurogenesis / Q000276:immunology; D011837:Radiation-Protective Agents / Q000494:pharmacology* / Q000627:therapeutic use
C000714847:Dcx protein, mouse; D000089662:Doublecortin Protein; D011837:Radiation-Protective Agents; D004999:Amifostine