Severe mitochondrial damage associated with low-dose radiation sensitivity in ATM- and NBS1-deficient cells
Open accessAbstract
Low-dose radiation risks remain unclear owing to a lack of sufficient studies. We previously reported that low-dose, long-term fractionated radiation (FR) with 0.01 or 0.05 Gy/fraction for 31 d inflicts oxidative stress in human fibroblasts due to excess levels of mitochondrial reactive oxygen species (ROS). To identify the small effects of low-dose radiation, we investigated how mitochondria respond to low-dose radiation in radiosensitive human ataxia telangiectasia mutated (ATM)- and Nijmegen breakage syndrome (NBS)1-deficient cell lines compared with corresponding cell lines expressing ATM and NBS1. Consistent with previous results in normal fibroblasts, low-dose, long-term FR increased mitochondrial mass and caused accumulation of mitochondrial ROS in ATM- and NBS1-complemented cell lines. Excess mitochondrial ROS resulted in mitochondrial damage that was in turn recognized by Parkin, leading to mitochondrial autophagy (mitophagy). In contrast, ATM- and NBS1-deficient cells showed defective induction of mitophagy after low-dose, long-term FR, leading to accumulation of abnormal mitochondria; this was determined by mitochondrial fragmentation and decreased mitochondrial membrane potential. Consequently, apoptosis was induced in ATM- and NBS1-deficient cells after low-dose, long-term FR. Antioxidant N-acetyl-L-cysteine was effective as a radioprotective agent against mitochondrial damage induced by low-dose, long-term FR among all cell lines, including radiosensitive cell lines. In conclusion, we demonstrated that mitochondria are target organelles of low-dose radiation. Mitochondrial response influences radiation sensitivity in human cells. Our findings provide new insights into cancer risk estimation associated with low-dose radiation exposure.
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Low doses of radiation trigger severe mitochondrial damage.
“Low doses of radiation trigger severe mitochondrial damage (Shimura et al., 2016) and the lower diffusion rates of solutes in microgravity (Smith et al., 2009) reduce the hydrogen gradient at the mitochondrial intermembrane space, reducing electron transport chain and ATP synthesis (Nelson, 2013).”
From Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact (2020) · cites this paper as Shimura et al., 2016
The section on mitochondria as targets of low-dose radiation reports severe mitochondrial damage in radiosensitive cell lines, while ATM- and NBS1-complemented cells showed mitochondrial ROS-mediated oxidative stress. The Abstract specifies a low-dose, long-term fractionated-radiation regimen. The claim omits those conditions and implies that low doses generally trigger severe mitochondrial damage. (LLM, conf=0.88)
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- Authors
- Shimura, T., Kobayashi, J., Komatsu, K., & Kunugita, N.
- Affiliations
- National Institute of Public Health (JP)
- Kyoto University (JP)
- Corresponding author
- Shimura, Tsutomu
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2016-03-03
- Volume
- 15
- Issue
- 8
- Pages
- 1099-1107
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC4889229
- OpenAlex
- W2296251088
- Cited by
- 55
- References
- 34
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 4 · 2021: 7 · 2020: 10 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 3
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (15K12220)
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- low-dose radiation, radiosensitivity, mitochondrial damage, ATM deficiency, ataxia telangiectasia, Nijmegen breakage syndrome, mitochondrial reactive oxygen species, oxidative stress, Parkin, mitophagy, mitochondrial fragmentation, mitochondrial membrane potential, apoptosis, N-acetylcysteine, radiation protection, cancer risk assessment
- MeSH terms
- Acetylcysteine, Cell Nucleus, Cell Survival, DNA Damage, Dose-Response Relationship, Radiation, Histones, Humans, Mitochondria, Models, Biological, Nuclear Proteins, Radiation Tolerance, Apoptosis, Reactive Oxygen Species, Cell Cycle Proteins, Membrane Potential, Mitochondrial, Mitophagy, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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