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电离辐射对晶状体中残留 53BP1 焦点的逆剂量率效应。

Inverse dose-rate effect of ionising radiation on residual 53BP1 foci in the eye lens.

机构信息

Public Health England, Centre for Radiation, Chemical and Environmental Hazards, Chilton, Didcot, Oxon, UK.

Durham University, Department of Biosciences, Durham, UK.

出版信息

Sci Rep. 2019 Jul 18;9(1):10418. doi: 10.1038/s41598-019-46893-3.

DOI:10.1038/s41598-019-46893-3
PMID:31320710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6639373/
Abstract

The influence of dose rate on radiation cataractogenesis has yet to be extensively studied. One recent epidemiological investigation suggested that protracted radiation exposure increases radiation-induced cataract risk: cumulative doses of radiation mostly <100 mGy received by US radiologic technologists over 5 years were associated with an increased excess hazard ratio for cataract development. However, there are few mechanistic studies to support and explain such observations. Low-dose radiation-induced DNA damage in the epithelial cells of the eye lens (LECs) has been proposed as a possible contributor to cataract formation and thus visual impairment. Here, 53BP1 foci was used as a marker of DNA damage. Unexpectedly, the number of 53BP1 foci that persisted in the mouse lens samples after γ-radiation exposure increased with decreasing dose-rate at 4 and 24 h. The C57BL/6 mice were exposed to 0.5, 1 and 2 Gy ƴ-radiation at 0.063 and 0.3 Gy/min and also 0.5 Gy at 0.014 Gy/min. This contrasts the data we obtained for peripheral blood lymphocytes collected from the same animal groups, which showed the expected reduction of residual 53BP1 foci with reducing dose-rate. These findings highlight the likely importance of dose-rate in low-dose cataract formation and, furthermore, represent the first evidence that LECs process radiation damage differently to blood lymphocytes.

摘要

辐射白内障ogenesis 的剂量率影响尚未得到广泛研究。最近的一项流行病学调查表明,长时间的辐射暴露会增加辐射诱导白内障的风险:在 5 年内,美国放射技师接受的辐射累积剂量大多<100 mGy,与白内障发展的超额危害比增加有关。然而,很少有机制研究来支持和解释这些观察结果。眼晶状体(LEC)上皮细胞中的低剂量辐射诱导的 DNA 损伤被认为是白内障形成和视力障碍的一个可能原因。在这里,53BP1 焦点被用作 DNA 损伤的标志物。出乎意料的是,在γ辐射暴露后,在 4 和 24 小时时,在小鼠晶状体样本中持续存在的 53BP1 焦点的数量随着剂量率的降低而增加。C57BL/6 小鼠在 0.063 和 0.3 Gy/min 的 0.5、1 和 2 Gy γ 射线下以及在 0.014 Gy/min 的 0.5 Gy 下进行照射。这与我们从相同动物组中收集的外周血淋巴细胞的数据形成对比,后者显示出预期的残留 53BP1 焦点随剂量率降低而减少。这些发现强调了剂量率在低剂量白内障形成中的重要性,此外,还代表了第一个证据,即 LEC 对辐射损伤的处理与血淋巴细胞不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/611f8f9cfbd6/41598_2019_46893_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/ad37877aee44/41598_2019_46893_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/208d7ba536aa/41598_2019_46893_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/611f8f9cfbd6/41598_2019_46893_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/ad37877aee44/41598_2019_46893_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/208d7ba536aa/41598_2019_46893_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5641/6639373/611f8f9cfbd6/41598_2019_46893_Fig3_HTML.jpg

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