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Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation.

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.
AuthorsHae-June Lee, Joong-Sun Kim, Myoung-Sub Song, Heung-Sik Seo, Miyoung Yang, Jong Choon Kim, Sung-Kee Jo, Taekyun Shin, Changjong Moon, Sung-Ho Kim
JournalJournal of veterinary science (J Vet Sci) Vol. 11 Issue 1 Pg. 81-3 (Mar 2010) ISSN: 1976-555X [Electronic] Korea (South)
PMID20195069 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Dcx protein, mouse
  • Doublecortin Protein
  • Radiation-Protective Agents
  • Amifostine
Topics
  • Acute Radiation Syndrome (drug therapy, immunology, psychology)
  • Amifostine (pharmacology, therapeutic use)
  • Animals
  • Apoptosis (immunology)
  • Doublecortin Protein
  • 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)

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