Ionizing radiation induced cataracts: Recent biological and mechanistic developments and perspectives for future research

Ainsbury, Elizabeth A.; Barnard, Stephen; Bright, Scott J.; Dalke, Claudia; Jarrı́n, Miguel; Kunze, Sarah; Tanner, R.J.; Dynlacht, Joseph R.; Quinlan, Roy A.; Graw, Jochen; Kadhim, Munira; Hamada, Nobuyuki

doi:10.1016/j.mrrev.2016.07.010

Cited by 112 publications

(78 citation statements)

References 255 publications

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“…Consideration of recent epidemiological evidence led ICRP to recommend in 2011 a threshold of 0.5 Gy (independent of rate of dose delivery and assuming progression of detectable opacities into vision-impairing cataracts) and an occupational equivalent dose limit for the lens of 20 mSv/year, averaged over defined periods of 5 years, with no single year exceeding 50 mSv): these are significant reductions from previously recommendations (i.e., a threshold for detectable opacities of 0.5–2 Gy for acute exposure and 5 Gy for highly fractionated or protracted exposures, a threshold for vision-impairing cataracts of 2–10 Gy for acute exposure and >8 Gy for highly fractionated or protracted exposures, and an occupational equivalent dose limit for the lens of 150 mSv/year) [6,7]. Thus, the lens is now considered much more radiosensitive than previously thought, but its mechanisms remain incompletely understood [8,9]. …”

Section: Introductionmentioning

confidence: 99%

Ionizing radiation response of primary normal human lens epithelial cells

Hamada

2017

PLoS ONE

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Whilst the cataractogenic potential of ionizing radiation has been known for over the past 120 years, little is known about radiation responses of lens cells. Our previous work was the first to evaluate the radiosensitivity of lens cells with the clonogenic assay, documenting that the survival of HLEC1 human lens epithelial cells is comparable to that of WI-38 human lung fibroblasts. Moreover, HLEC1 cells were found to contain subsets where irradiation stimulates proliferation or facilitates formation of abortive colonies with fewer cells than human fibroblasts. This study aims to gain insights into these mechanisms. Irradiation of HLEC1 cells with 10% survival dose caused a growth delay but did not reduce viability. HLEC1 cells at high cumulative population doubling level were more susceptible to radiogenic premature senescence than WI-38 cells. Concerning p53 binding protein 1 (53BP1) foci, HLEC1 cells harbored less spontaneous foci but more radiogenic foci than in WI-38 cells, and the focus number returned to spontaneous levels within 48 h postirradiation both in HLEC1 and WI-38. The chemical inhibition of DNA repair kinases ataxia telangiectasia mutated, DNA-dependent protein kinase or both delayed and attenuated the appearance and disappearance of radiogenic 53BP1 foci, increased radiogenic premature senescence and enhanced clonogenic inactivation. The DNA microarray analysis suggested both radiogenic stimulation and inhibition of cell proliferation. Treatment with conditioned medium from irradiated cells did not change growth and the plating efficiency of nonirradiated cells. These results partially explain mechanisms of our previous observations, such that unrepaired or incompletely repaired DNA damage causes a growth delay in a subset of HLEC1 cells without changing viability through induction of premature senescence, thereby leading to clonogenic inactivation, but that growth is stimulated in another subset via as yet unidentified mechanisms, warranting further studies.

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Section: Introductionmentioning

confidence: 99%

Ionizing radiation response of primary normal human lens epithelial cells

Hamada

2017

PLoS ONE

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“…Hladik and Tapio review the epidemiology and biology of brain effects [3]. Shore provides an overview of cataract epidemiology [4], whereas Ainsbury et al reviews the biology of cataractogenesis following low linear energy transfer (LET) radiation exposures [5]; Hamada and Sato also review high-LET radiation cataractogenesis [6]. Grubber and Dörr consider the radiobiology of the oral mucosa, which is important in light of the adverse reactions to radiotherapy [7].…”

Section: Introductionmentioning

confidence: 99%

Special issue: Tissue reactions to ionizing radiation exposure

Hamada

Bouffler

Woloschak

2016

Mutation Research/Reviews in Mutation Research

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“…Recent epidemiologic studies have yielded new evidence of radiation-induced cataract at lower doses (16), leading the International Commission on Radiological Protection to lower the assumed threshold to 0.5 Gy (17). However, investigators in some literature reviews focused on more recent epidemiologic and biologic study findings (18,19) have questioned whether the data are still consistent with the theory that cataract is a tissue reaction and have described potential stochastic phenomena linked to DNA damage as an explanation for the increased risks at lower radiation…”

Section: Us Radiologic Technologist Cohortmentioning

confidence: 99%

Cataract Risk in a Cohort of U.S. Radiologic Technologists Performing Nuclear Medicine Procedures

et al. 2018

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Purpose To estimate the risk of cataract in a cohort of nuclear medicine (NM) radiologic technologists on the basis of their work histories and radiation protection practices. Materials and Methods In the years 2003-2005 and 2012-2013, 42 545 radiologic technologists from a U.S. prospective study completed questionnaires in which they provided information regarding their work histories and cataract histories. Cox proportional hazards models, stratified according to birth-year cohort (born before 1940 or born in 1940 or later) and adjusted for age, sex, and race, were used to estimate hazard ratios (HRs) for the risk of cataract in radiologic technologists according to NM work history practices according to decade. Results During the follow-up period (mean follow-up, 7½ years), 7137 incident cataracts were reported. A significantly increased risk of cataract (HR, 1.08; 95% confidence interval [CI]: 1.03, 1.14) was observed among workers who performed an NM procedure at least once-as opposed to never. Risks of cataract were increased in the group who had performed a diagnostic (HR, 1.07; 95% CI: 1.01, 1.12) or therapeutic (HR, 1.10; 95% CI: 1.04, 1.17) NM procedure. Risks were higher for those who had first performed diagnostic NM procedures in the 1980s to early 2000s (HR, 1.30; 95% CI: 1.08, 1.58) and those who had performed therapeutic NM procedures in the 1970s (HR, 1.11; 95% CI: 1.01, 1.23) and in the 1980s to early 2000s (HR, 1.14; 95% CI: 1.02, 1.29). With the exception of a significantly increased risk associated with performing therapeutic NM procedures without shielding the radiation source in the 1980s (HR, 1.32; 95% CI: 1.04, 1.67), analyses revealed no association between cataract risk and specific radiation protection technique used. Conclusion An increased risk of cataract was observed among U.S. radiologic technologists who had performed an NM procedure at least once. This association should be examined in future studies incorporating estimated lens doses. RSNA, 2017.

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Ionizing radiation induced cataracts: Recent biological and mechanistic developments and perspectives for future research

Cited by 112 publications

References 255 publications

Ionizing radiation response of primary normal human lens epithelial cells

Ionizing radiation response of primary normal human lens epithelial cells

Special issue: Tissue reactions to ionizing radiation exposure

Cataract Risk in a Cohort of U.S. Radiologic Technologists Performing Nuclear Medicine Procedures

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