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Radiation‐induced cataracts
Author(s) -
Barnard S.,
Moquet J.,
Lloyd S.,
Ellender M.,
Ainsbury E.,
Quinlan R.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.03682
Subject(s) - ionizing radiation , cataracts , epithelium , dna damage , lens (geology) , biology , microbiology and biotechnology , retinal pigment epithelium , staining , pathology , cancer research , irradiation , retina , medicine , dna , genetics , physics , paleontology , neuroscience , nuclear physics
Summary The radiosensitive nature of the lens has been increasingly reported, although the exact mechanistic details of the radiation response pathways for cataractogenesis are unclear. Radiation‐induced DNA damage and the subsequent impairment of repair pathways within the lens epithelium are involved. Here, two distinct regions of the murine lens epithelium have been analysed for their differences in double strand break ( DSB ) repair responses to ionising radiation. The responses of epithelial cells located at the anterior pole (central region) have been compared to those in other locations, including the proliferative compartment, and including the very periphery of the monolayer (peripheral region). Described here are the responses between the two regions, across four strains, over a low dose (0–25 mG y) X‐irradiation range up to 24 hours. Damage visualised through biomarker 53 BP 1 staining was present across the epithelium, repair kinetics appear non‐uniform. Epithelial cells in the central region have significantly more 53 BP 1 positive foci. In this study, BALB /c were identified as the most suitable strain for low dose ionising radiation exposure investigation.