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Roles of nitric oxide in adaptive response induced in zebrafish embryos in vivo by microbeam protons

机译:一氧化氮在微束质子体内诱导斑马鱼胚胎适应性反应中的作用

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摘要

Radioadaptive response (RAR) was successfully induced in dechorionated (5 h post-fertilization, hpf) embryos of the zebrafish, Danio rerio, by 3.4 MeV protons from the microbeam irradiation facility (Single-Particle Irradiation System to Cell, acronym as SPICE) [ ] at the National Institute of Radiological Sciences (NIRS), against a challenging exposure of 2 Gy of X-ray irradiation at 10 hpf. The RAR induction was corroborated by reduced apoptotic signals at 25 hpf revealed through terminal dUTP transferase-mediated nick end-labeling assay. If de novo synthesis of factors was required for RAR induction, these should have already been synthesized at 5 h after the priming dose.Application of a nitric oxide scavenger 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) to the medium at 0, 1, 2, 3 or 5 h after application of priming exposure significantly suppressed RAR. The suppression of RAR with the application of cPTIO to the medium at 5 h after the priming dose irradiation, where de novo synthesis of factors should have been completed, suggested that NO scavenging impaired the repair machineries in the bystander cells. The suppression of RAR with the application of cPTIO to the medium at earlier than 5 h after the priming dose irradiation could be explained by the scavenging of bystander NO signals in the medium and thus deterring the de novo synthesis of factors.
机译:通过微束辐照设备(单颗粒辐照系统对细胞,缩写为SPICE)产生的3.4 MeV质子,成功地在斑马鱼Danio rerio的去绒毛化(受精后5 h,hpf)胚胎中诱导了放射自适应反应[RAR] [美国国家放射科学研究院(NIRS)的研究,以10 hpf的2 Gy的X射线辐照挑战性暴露。通过末端dUTP转移酶介导的缺口末端标记测定法揭示的25 hpf的凋亡信号降低,证实了RAR的诱导作用。如果需要从头合成新的因子来诱导RAR,则应在初次给药后5小时合成这些因子。一氧化氮清除剂2-(4-羧苯基)-4,4,5,5-四甲基咪唑啉-在施加底漆暴露后的0、1、2、3或5小时,向介质中添加1-oxyl-3-oxide(cPTIO)可显着抑制RAR。在初次剂量照射后5 h将cPTIO施加到培养基上即可完成RAR的抑制作用,此时应该完成从头开始的因子合成,这表明NO清除会削弱旁观者细胞的修复机制。在引发剂量照射后5 h之前,将cPTIO施加至培养基可抑制RAR,其原因可能是清除培养基中旁观者NO信号,从而阻止了因子的从头合成。

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