ArticleCell cycle (Georgetown, Tex.)2016
Severe mitochondrial damage associated with low-dose radiation sensitivity in ATM- and NBS1-deficient cells.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Radiotherapy-Induced Side Effects: Epidemiology, Pathogenesis, Prevention and Treatments.MedComm · 2026Review
- Gadolinium-Doped Iron Oxide Nanoparticles Enhance Radiosensitivity in Melanoma Models Associated with Metabolic Dysfunction.Pharmaceutics · 2026Article
- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure.JBMR plus · 2025Article
- Effects of low-dose radiation produced during radiofrequency ablation guided by 3D mapping on mitochondrial apoptosis in diabetic cardiomyocytes.BMC cardiovascular disorders · 2025Article
- The interplay between DNA damage response and mitochondrial dysfunction in radiotherapy.Frontiers in oncology · 2025Review
- A NovelMicroorganisms · 2024Article
- Radiation-Induced miRNAs Changes and cf mtDNA Level in Trauma Surgeons: Epigenetic and Molecular Biomarkers of X-ray Exposure.International journal of molecular sciences · 2024Article
- Cosmic kidney disease: an integrated pan-omic, physiological and morphological study into spaceflight-induced renal dysfunction.Nature communications · 2024Article
- The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation.Cells · 2024Review
- Article
- Review
- Differential Expression of ATM, NF-KB, PINK1 and Foxo3a in Radiation-Induced Basal Cell Carcinoma.International journal of molecular sciences · 2023Article
- Manipulation of Redox Metabolism Using Pharmacologic Ascorbate Opens a Therapeutic Window for Radio-Sensitization by ATM Inhibitors in Colorectal Cancer.International journal of radiation oncology, biology, physics · 2023Article
- Radiation affects glutathione redox reaction by reduced glutathione peroxidase activity in human fibroblasts.Journal of radiation research · 2022Article
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
- MHY1485 enhances X-irradiation-induced apoptosis and senescence in tumor cells.Journal of radiation research · 2021Article
- Review
- The role of mitochondrial oxidative stress and the tumor microenvironment in radiation-related cancer.Journal of radiation research · 2021Review
- DNA damage and mitochondria in cancer and aging.Carcinogenesis · 2020Review
- Mechanism of turnover or persistence of radiation-induced myofibroblast in vitro.Cell cycle (Georgetown, Tex.) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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