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KMID : 0893420100110010081
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Journal of Veterinary Science
2010 Volume.11 No. 1 p.81 ~ p.83
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Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation
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Lee Hae-June
Kim Joong-Sun
Song Myoung-Sub
Seo Heung-Sik
Yang Mi-Young
Kim Jong-Choon
Jo Sung-Kee
Shin Taek-Yun
Moon Chang-Jong
Kim Seong-Ho
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Abstract
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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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KEYWORD
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acute radiation syndrome, amifostine, hippocampus, memory impairment, neurogenesis
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