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低剂量电离辐射的生物行为学、神经免疫影响。

The biobehavioral and neuroimmune impact of low-dose ionizing radiation.

机构信息

Department of Animal Sciences, University of Illinois, Urbana, IL, USA.

出版信息

Brain Behav Immun. 2012 Feb;26(2):218-27. doi: 10.1016/j.bbi.2011.09.006. Epub 2011 Sep 21.

DOI:10.1016/j.bbi.2011.09.006
PMID:21958477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3264777/
Abstract

In the clinical setting, repeated exposures (10-30) to low-doses of ionizing radiation (≤200 cGy), as seen in radiotherapy for cancer, causes fatigue. Almost nothing is known, however, about the fatigue inducing effects of a single exposure to environmental low-dose ionizing radiation that might occur during high-altitude commercial air flight, a nuclear reactor accident or a solar particle event (SPE). To investigate the short-term impact of low-dose ionizing radiation on mouse biobehaviors and neuroimmunity, male CD-1 mice were whole body irradiated with 50 cGy or 200 cGy of gamma or proton radiation. Gamma radiation was found to reduce spontaneous locomotor activity by 35% and 36%, respectively, 6 h post irradiation. In contrast, the motivated behavior of social exploration was un-impacted by gamma radiation. Examination of pro-inflammatory cytokine gene transcripts in the brain demonstrated that gamma radiation increased hippocampal TNF-α expression as early as 4 h post-irradiation. This was coupled to subsequent increases in IL-1RA (8 and 12 h post irradiation) in the cortex and hippocampus and reductions in activity-regulated cytoskeleton-associated protein (Arc) (24 h post irradiation) in the cortex. Finally, restraint stress was a significant modulator of the neuroimmune response to radiation blocking the ability of 200 cGy gamma radiation from impairing locomotor activity and altering the brain-based inflammatory response to irradiation. Taken together, these findings indicate that low-dose ionizing radiation rapidly activates the neuroimmune system potentially causing early onset fatigue-like symptoms in mice.

摘要

在临床环境中,如癌症放射治疗中所见,反复暴露于低剂量电离辐射(≤200 毫戈瑞)会导致疲劳。然而,对于单次暴露于环境低剂量电离辐射(可能发生在高空商业航班、核反应堆事故或太阳粒子事件中)引起疲劳的影响,几乎一无所知。为了研究低剂量电离辐射对小鼠生物行为和神经免疫的短期影响,雄性 CD-1 小鼠接受 50 毫戈瑞或 200 毫戈瑞γ射线或质子辐射全身照射。结果发现,γ 射线分别使辐照后 6 小时的自发运动活性降低 35%和 36%。相比之下,γ 射线对社交探索的动机行为没有影响。对大脑中促炎细胞因子基因转录本的检查表明,γ 射线早在辐照后 4 小时就增加了海马 TNF-α 的表达。这与随后皮质和海马中 IL-1RA 的增加(辐照后 8 和 12 小时)以及皮质中活性调节细胞骨架相关蛋白(Arc)的减少(辐照后 24 小时)有关。最后,束缚应激是辐射引起的神经免疫反应的一个重要调节剂,阻止 200 毫戈瑞γ射线辐照损害运动活动和改变大脑炎症反应。总之,这些发现表明,低剂量电离辐射会迅速激活神经免疫系统,可能导致小鼠出现早期疲劳样症状。

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