Even low doses of radiation lead to DNA damage accumulation in lung tissue according to the genetically-defined DNA repair capacity
| Autor: | Elias Flockerzi, Stefanie Schanz, Claudia E. Rübe |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Genetic Markers
Pathology medicine.medical_specialty DNA Repair Chromosomal Proteins Non-Histone DNA damage DNA repair medicine.medical_treatment Biology Ionizing radiation Mice 03 medical and health sciences 0302 clinical medicine Parenchyma medicine Animals Humans DNA Breaks Double-Stranded Radiology Nuclear Medicine and imaging Lung 030304 developmental biology 0303 health sciences Dose fractionation Dose-Response Relationship Radiation Lung Injury Hematology respiratory system 3. Good health DNA-Binding Proteins Radiation therapy Disease Models Animal Radiation Injuries Experimental medicine.anatomical_structure Oncology Apoptosis 030220 oncology & carcinogenesis Tumor Suppressor p53-Binding Protein 1 |
| Zdroj: | Radiotherapy and Oncology |
| ISSN: | 0167-8140 |
| DOI: | 10.1016/j.radonc.2014.03.011 |
| Popis: | 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 10weeks of daily low-dose 100-mGy radiation. Results 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. Conclusion 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. |
| Databáze: | OpenAIRE |
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