Inverse dose-rate effect of ionising radiation on residual 53BP1 foci in the eye lens
Barnard, SGR; McCarron, R; Moquet, J; Quinlan, RA; Ainsbury, E
Professor Roy Quinlan firstname.lastname@example.org
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.
Barnard, S., McCarron, R., Moquet, J., Quinlan, R., & Ainsbury, E. (2019). Inverse dose-rate effect of ionising radiation on residual 53BP1 foci in the eye lens. Scientific Reports, 9, Article 10418. https://doi.org/10.1038/s41598-019-46893-3
|Journal Article Type||Article|
|Acceptance Date||Jul 2, 2019|
|Online Publication Date||Jul 18, 2019|
|Deposit Date||Jul 10, 2019|
|Publicly Available Date||Jul 19, 2019|
|Peer Reviewed||Peer Reviewed|
Published Journal Article
Publisher Licence URL
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.