Background and purpose
Intensity-modulated radiation therapy for thoracic malignancies increases the exposure of healthy lung tissue to low-dose radiation. The biological impact of repetitive low-dose radiation on the radiosensitive lung is unclear.
Materials and methods
In the present study, using mouse strains with different genetic DNA repair capacities, we monitored the extent of DNA damage in lung parenchyma after 2, 4, 6, 8, and 10 weeks of daily low-dose 100-mGy radiation.
Using 53BP1 as a marker for double-strand breaks, we observed DNA damage accumulation during fractionated low-dose radiation with increasing cumulative doses. The amount of radiation-induced 53BP1 varied significantly between bronchiolar and alveolar epithelial cells, suggesting that different cell populations in the lung parenchyma had varying vulnerabilities to ionizing radiation. The genetic background of DNA repair determined the extent of cumulative low-dose radiation damage. Moreover, increased DNA damage during fractionated low-dose radiation affected replication, and apoptosis in the lung parenchyma, which may influence overall lung function.
Collectively, our results suggest that low, yet damaging, doses of radiation increase the risk of toxicity to normal lung tissue and the probability of developing secondary malignancies.
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Published online: April 21, 2014
Accepted: March 18, 2014
Received in revised form: January 10, 2014
Received: October 24, 2013
© 2014 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.