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.
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Authors | Hae-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 |
Journal | Journal of veterinary science
(J Vet Sci)
Vol. 11
Issue 1
Pg. 81-3
(Mar 2010)
ISSN: 1976-555X [Electronic] Korea (South) |
PMID | 20195069
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Dcx protein, mouse
- Doublecortin Protein
- Radiation-Protective Agents
- Amifostine
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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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