Wang B, Ohyama H, Haginoya K, Odaka T, Itsukaichi H, Yukawa O, Yamada T, Hayata I
Division of Radiobiology and Biodosimetry, National Institute of Radiological Sciences, Anagawa 4-9-1, Inage-ku, Chiba 263-8555, Japan.
Radiat Res. 2000 Sep;154(3):277-82. doi: 10.1667/0033-7587(2000)154[0277:arieir]2.0.co;2.
We reported previously that a radiation-induced adaptive response existed in the late period of embryogenesis, and that radiation-induced apoptosis in the predigital regions was responsible for digital defects in embryonic ICR mice. To investigate the possible involvement of the Trp53 gene and radiation-induced apoptosis in radiation-induced adaptive responses in embryogenesis, the present study was conducted using Trp53 wild-type (Trp53(+/+)) and Trp53 heterozygous (Trp53(+/-)) embryonic mice of the C57BL/6 strain. The existence of a radioadaptive response in the Trp53(+/+) embryonic mice was demonstrated by irradiating the embryos with 5 or 30 cGy on embryonic day 11 prior to a challenging irradiation at 3 Gy on embryonic day 12. The two conditioning doses at 5 and 30 cGy significantly suppressed the induction of apoptosis by the challenging dose in the predigital regions of limb buds in the Trp53(+/+) embryonic mice, while no such effect was found in the Trp53(+/-) embryonic mice. These findings indicate that induction of a radioadaptive response in embryogenesis is related to Trp53 gene status and the occurrence of radiation-induced apoptosis.
我们之前报道过,辐射诱导的适应性反应存在于胚胎发育后期,并且辐射诱导的指前区域凋亡是导致ICR胚胎小鼠出现指畸形的原因。为了研究Trp53基因和辐射诱导的凋亡在胚胎发育辐射诱导适应性反应中可能的作用,本研究使用C57BL/6品系的Trp53野生型(Trp53(+/+))和Trp53杂合型(Trp53(+/-))胚胎小鼠进行。通过在胚胎第11天用5或30 cGy照射胚胎,然后在胚胎第12天用3 Gy进行挑战性照射,证实了Trp53(+/+)胚胎小鼠中存在辐射适应性反应。5和30 cGy这两个预处理剂量显著抑制了挑战性剂量在Trp53(+/+)胚胎小鼠肢芽指前区域诱导的凋亡,而在Trp53(+/-)胚胎小鼠中未发现这种效应。这些发现表明,胚胎发育中辐射适应性反应的诱导与Trp53基因状态以及辐射诱导凋亡的发生有关。