Assessment of cellular dose and damage induced by radon and its progeny using the BEAS-2B cell mesh model

被引:0
|
作者
Gao, Han [1 ]
Wang, Yidi [1 ]
Guo, Jiahao [1 ]
Xue, Huiyuan [1 ]
Wang, Xinjie [1 ]
Yan, Kaijin [1 ]
Wu, Tao [1 ]
Gao, Xiaotong [1 ]
Li, Haiyang [2 ]
Sun, Liang [1 ]
机构
[1] Soochow Univ, State Key Lab Radiat Med & Protect, Collaborat Innovat Ctr Radiol Med, Jiangsu Higher Educ Inst,Sch Radiat Med & Protect, Suzhou 215123, Peoples R China
[2] Nanjing Med Univ, Binhai Cty Peoples Hosp, Radiotherapy Dept, Kangda Coll, Yancheng, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Cellular S -Values; Radon; PHITS; Cell mesh model; DSB; TARGETED RADIONUCLIDE THERAPY; MONTE-CARLO-SIMULATION; DNA-DAMAGE; S-VALUES; DOSIMETRY; EXPOSURE; ENERGY; RADIOIMMUNOTHERAPY; SOLUBILITY; LEUKEMIA;
D O I
10.1016/j.apradiso.2025.111749
中图分类号
O61 [无机化学];
学科分类号
070301 ; 081704 ;
摘要
The decay of radon and its progeny mainly produces alpha particles and beta particles. Due to their short range and high linear energy transfer (LET) of alpha particles, it is necessary to evaluate the dose deposition at the cellular and subcellular levels so as to better assess their health effects on the human body. Given that the lung is the primary target organ for radon exposure, we utilized human bronchial epithelial cells (BEAS-2B cells) to construct a realistic mesh model. Using Monte Carlo simulation software PHITS, we computed cellular S-values under conditions of radon and progeny irradiation, the deposited does inside cells of nuclide that distribute outside cells has been calculated. These calculations were contrasted with results obtained from traditional geometric models and MIRDcell calculations. To quantify the damage effects caused by radon and its progeny, this study used MCDS to calculate the DNA damage, for various nuclides, Rn-222 produces the highest number of double-strand breaks (DSBs) up to 21.8 Gy-1cell-1, while Tl-210 produces the least DSBs with 8.32 Gy-1cell-1. Additionally, other damage metrics such as single-strand breaks (SSBs), "OTHER", and "ALL CLUSTERS" were quantified. This research, based on the BEAS-2B cell model, offers more precise information on cellular doses and damage effects of radon and its progeny. It holds significant implications for the future development of radiation protection strategies and applications in radon therapy.
引用
收藏
页数:10
相关论文
共 50 条
  • [21] Toxicity mechanism of acrolein on DNA damage and apoptosis in BEAS-2B cells: Insights from cell biology and molecular docking analyses
    Liu, Dan
    Cheng, Ye
    Tang, Zhipeng
    Mei, Xueying
    Cao, Xiangyu
    Liu, Jianli
    TOXICOLOGY, 2022, 466
  • [22] Mitochondrial OGG1 protects against PM2.5-induced oxidative DNA damage in BEAS-2B cells
    Yang, Lawei
    Wang, Yahong
    Lin, Ziying
    Zhou, Xu
    Chen, Ting
    He, Huijuan
    Huang, Haili
    Yang, Teng
    Jiang, Yun
    Xu, Wenya
    Yao, Weimin
    Liu, Tie
    Liu, Gang
    EXPERIMENTAL AND MOLECULAR PATHOLOGY, 2015, 99 (02) : 365 - 373
  • [23] RUNX2/miR-31/SATB2 pathway in nickel-induced BEAS-2B cell transformation
    Zhu, Yusha
    Chen, Qiao Yi
    Jordan, Ashley
    Sun, Hong
    Roy, Nirmal
    Costa, Max
    ONCOLOGY REPORTS, 2021, 46 (02)
  • [24] Oxidative potential of water- soluble PM1 and induced oxidative stress in BEAS-2B cell line
    Melzi, G.
    Massimi, L.
    Rinaldi, M.
    Paglione, M.
    Tarallo, N.
    Crova, F.
    Frezzini, M. A.
    Valli, G.
    Canepari, S.
    Decesari, S.
    Vecchi, R.
    Marinovich, M.
    Corsini, E.
    TOXICOLOGY LETTERS, 2023, 384 : S171 - S171
  • [25] Gene profiles of a bronchial epithelial cell line (BEAS-2B) induced by exposure to low-molecular weight chemicals
    Remy, S.
    Nelissen, I.
    Hooyberghs, J.
    Van den Heuvel, R.
    Schoeters, G.
    TOXICOLOGY LETTERS, 2011, 205 : S279 - S279
  • [26] Low-dose combined exposure of carboxylated black carbon and heavy metal lead induced potentiation of oxidative stress, DNA damage, inflammation, and apoptosis in BEAS-2B cells
    Jiang, Nan
    Wen, Haiyan
    Zhou, Meng
    Lei, Tiantian
    Shen, Jianyun
    Zhang, Di
    Wang, Rong
    Wu, Hai
    Jiang, Shuanglin
    Li, Wenyong
    ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 2020, 206
  • [27] Tiotropium/Olodaterol treatment reduces cigarette smoke extract-induced cell death in BEAS-2B bronchial epithelial cells
    Chen, Cheng-hsiung
    Li, Yi-Rong
    Lin, Sheng-Hao
    Chang, Hsiu-Hui
    Chai, Woei-Horng
    Chan, Po-Chiang
    Lin, Ching-Hsiung
    BMC PHARMACOLOGY & TOXICOLOGY, 2020, 21 (01):
  • [28] Long-term exposures to low doses of titanium dioxide nanoparticles induce cell transformation, but not genotoxic damage in BEAS-2B cells
    Vales, Gerard
    Rubio, Laura
    Marcos, Ricard
    NANOTOXICOLOGY, 2015, 9 (05) : 568 - 578
  • [29] Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells
    Jing Wu
    Yanfeng Shi
    Collins Otieno Asweto
    Lin Feng
    Xiaozhe Yang
    Yannan Zhang
    Hejing Hu
    Junchao Duan
    Zhiwei Sun
    Environmental Science and Pollution Research, 2017, 24 : 25071 - 25081
  • [30] mTORC1-TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells
    Ouyang, Di
    Xiong, Yiren
    Hu, Zuqing
    He, Jiayi
    He, Shanshan
    Liu, Renyi
    Gao, Zhenjie
    Hu, Dalin
    TOXICOLOGY, 2024, 504