J Vet Sci.  2010 Mar;11(1):81-83. 10.4142/jvs.2010.11.1.81.

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

Affiliations
  • 1Korea Institute of Radiological and Medical Science, Seoul 139-240, Korea.
  • 2College of Veterinary Medicine and Animal Medical Institute, Chonnam National University, Gwangju 500-757, Korea. moonc@chonnam.ac.kr
  • 3Advanced Radiation Technology Institute, KAERI, Jeonbuk 580-185, Korea.
  • 4College of Veterinary Medicine Jeju National University, Jeju 690-756, Korea.

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.

Keyword

acute radiation syndrome; amifostine; hippocampus; memory impairment; neurogenesis

MeSH Terms

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

Figure

  • Fig. 1 Pretreatment of amifosine significantly attenuates object recognition memory defects in mice with acute radiation syndrome (ARS). The sham controls (sham irradiation of 0 Gy), vehicle controls (vehicle + 2 Gy), and amifostine-treated mice (amifostine + 2 Gy) were examined (n = 7 for each group). *p < 0.05.

  • Fig. 2 Histological analyses for the sham controls (12 h after sham irradiation of 0 Gy), vehicle-treated, and amifostine-treated mouse hippocampe 12 h after gamma irradiation of 0.5 and 2 Gy. *p < 0.05, **p < 0.01.


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