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

作者：Lee Hae June; Kim Joong Sun; Song Myoung Sub; Seo Heung Sik; Yang Miyoung; Kim Jong Choon; Jo Sung Kee; Shin Taekyun; Moon Changjong^*; Kim Sung Ho

来源：Journal of Veterinary Science, 2010, 11(1): 81-83.

DOI：10.4142/jvs.2010.11.1.81

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

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 AIRS in adult mice, possibly by inhibiting a detrimental effect of irradiation on hippocampal neurogenesis.

• 出版日期2010-3