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中子未诱导斑马鱼胚胎产生辐射适应性反应。

Non-induction of radioadaptive response in zebrafish embryos by neutrons.

作者信息

Ng Candy Y P, Kong Eva Y, Kobayashi Alisa, Suya Noriyoshi, Uchihori Yukio, Cheng Shuk Han, Konishi Teruaki, Yu Kwan Ngok

机构信息

Department of Physics and Materials Science, City University of Hong Kong, Tat Chee Ave., Kowloon Tong, Hong Kong.

Research, Development and Support Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage, Chiba 263-8555, Japan Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.

出版信息

J Radiat Res. 2016 Jun;57(3):210-9. doi: 10.1093/jrr/rrv089. Epub 2016 Feb 4.

Abstract

In vivo neutron-induced radioadaptive response (RAR) was studied using zebrafish (Danio rerio) embryos. The Neutron exposure Accelerator System for Biological Effect Experiments (NASBEE) facility at the National Institute of Radiological Sciences (NIRS), Japan, was employed to provide 2-MeV neutrons. Neutron doses of 0.6, 1, 25, 50 and 100 mGy were chosen as priming doses. An X-ray dose of 2 Gy was chosen as the challenging dose. Zebrafish embryos were dechorionated at 4 h post fertilization (hpf), irradiated with a chosen neutron dose at 5 hpf and the X-ray dose at 10 hpf. The responses of embryos were assessed at 25 hpf through the number of apoptotic signals. None of the neutron doses studied could induce RAR. Non-induction of RAR in embryos having received 0.6- and 1-mGy neutron doses was attributed to neutron-induced hormesis, which maintained the number of damaged cells at below the threshold for RAR induction. On the other hand, non-induction of RAR in embryos having received 25-, 50- and 100-mGy neutron doses was explained by gamma-ray hormesis, which mitigated neutron-induced damages through triggering high-fidelity DNA repair and removal of aberrant cells through apoptosis. Separate experimental results were obtained to verify that high-energy photons could disable RAR. Specifically, 5- or 10-mGy X-rays disabled the RAR induced by a priming dose of 0.88 mGy of alpha particles delivered to 5-hpf zebrafish embryos against a challenging dose of 2 Gy of X-rays delivered to the embryos at 10 hpf.

摘要

利用斑马鱼(Danio rerio)胚胎研究了体内中子诱导的放射适应性反应(RAR)。日本国立放射科学研究所(NIRS)的用于生物效应实验的中子照射加速器系统(NASBEE)设施被用于提供2兆电子伏特的中子。选择0.6、1、25、50和100毫戈瑞的中子剂量作为预照射剂量。选择2戈瑞的X射线剂量作为激发剂量。斑马鱼胚胎在受精后4小时(hpf)去卵膜,在5 hpf接受选定的中子剂量照射,并在10 hpf接受X射线剂量照射。在25 hpf通过凋亡信号数量评估胚胎的反应。所研究的任何中子剂量均不能诱导RAR。接受0.6和1毫戈瑞中子剂量的胚胎中RAR未被诱导归因于中子诱导的兴奋效应,其将受损细胞数量维持在低于RAR诱导阈值的水平。另一方面,接受25、50和100毫戈瑞中子剂量的胚胎中RAR未被诱导可通过γ射线兴奋效应来解释,其通过触发高保真DNA修复以及通过凋亡清除异常细胞来减轻中子诱导的损伤。获得了单独的实验结果以验证高能光子可使RAR失效。具体而言,5或10毫戈瑞的X射线使在5 hpf给予斑马鱼胚胎0.88毫戈瑞α粒子预照射剂量并在10 hpf给予胚胎2戈瑞X射线激发剂量所诱导的RAR失效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bad/4915534/292b415615cd/rrv08901.jpg

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