1.Amifostine ameliorates recognition memory defect in acute radiation syndrome caused by relatively low-dose of gamma radiation.
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 of Veterinary Science 2010;11(1):81-83
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.
Acute Radiation Syndrome/drug therapy/*immunology/psychology
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Amifostine/*pharmacology/therapeutic use
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Animals
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Apoptosis/immunology
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Gamma Rays/*adverse effects
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Hippocampus/immunology
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Immunohistochemistry
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In Situ Nick-End Labeling
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Male
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Memory/*radiation effects
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Mice
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Mice, Inbred ICR
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Neurogenesis/immunology
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Radiation-Protective Agents/*pharmacology/therapeutic use