Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation
Journal of Veterinary Science
;
: 81-83, 2010.
Article
in English
| WPRIM
| ID: wpr-160869
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Radiation-Protective Agents
/
Immunohistochemistry
/
Apoptosis
/
Amifostine
/
In Situ Nick-End Labeling
/
Acute Radiation Syndrome
/
Neurogenesis
/
Gamma Rays
/
Hippocampus
/
Memory
Limits:
Animals
Language:
English
Journal:
Journal of Veterinary Science
Year:
2010
Type:
Article
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