Radiation-induced delayed bystander-type effects mediated by hemopoietic cells

Karen L. Burr, Joanne I. Robinson, Shubhra Rastogi, Michael T. Boylan, Philip J. Coates, Sally A. Lorimore, Eric G. Wright

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    Abstract

    Genetic lesions and cell death associated with exposure to ionizing radiation have generally been attributed to DNA damage arising as a consequence of deposition of energy in the cell nucleus. However, reports of radiation-induced bystander effects, in which DNA damage is produced in nonirradiated cells as a consequence of communication with irradiated cells, indicate additional mechanisms. At present, most information has been obtained using in vitro systems, and the in vivo significance of bystander factors is not clear. In this study we show that signals generated in vivo in the bone marrow of CBA/Ca mice irradiated with 4 Gy gamma rays 24 h previously, but not immediately postirradiation, are able to induce DNA damage and apoptosis in nonirradiated bone marrow cells. The signaling mechanism involves FasL, TNF-alpha, nitric oxide and superoxide and macrophages are implicated as a source of damaging signals. Such delayed bystander-type damage demonstrates the importance of studying tissue responses subsequent to the radiation exposure as well as effects at the time of irradiation when considering the mechanisms underlying the consequences of radiation exposures.
    Original languageEnglish
    Pages (from-to)760-8
    Number of pages9
    JournalRadiation Research
    Volume173
    Issue number6
    DOIs
    Publication statusPublished - 2010

    Fingerprint

    Bystander Effect
    DNA Damage
    Radiation
    damage
    deoxyribonucleic acid
    bone marrow
    radiation dosage
    radiation
    cells
    Inbred CBA Mouse
    Gamma Rays
    Radiation Effects
    Ionizing Radiation
    Cell Nucleus
    Superoxides
    Bone Marrow Cells
    macrophages
    inorganic peroxides
    Nitric Oxide
    apoptosis

    Cite this

    Burr, K. L., Robinson, J. I., Rastogi, S., Boylan, M. T., Coates, P. J., Lorimore, S. A., & Wright, E. G. (2010). Radiation-induced delayed bystander-type effects mediated by hemopoietic cells. Radiation Research, 173(6), 760-8. https://doi.org/10.1667/RR1937.1
    Burr, Karen L. ; Robinson, Joanne I. ; Rastogi, Shubhra ; Boylan, Michael T. ; Coates, Philip J. ; Lorimore, Sally A. ; Wright, Eric G. / Radiation-induced delayed bystander-type effects mediated by hemopoietic cells. In: Radiation Research. 2010 ; Vol. 173, No. 6. pp. 760-8.
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    abstract = "Genetic lesions and cell death associated with exposure to ionizing radiation have generally been attributed to DNA damage arising as a consequence of deposition of energy in the cell nucleus. However, reports of radiation-induced bystander effects, in which DNA damage is produced in nonirradiated cells as a consequence of communication with irradiated cells, indicate additional mechanisms. At present, most information has been obtained using in vitro systems, and the in vivo significance of bystander factors is not clear. In this study we show that signals generated in vivo in the bone marrow of CBA/Ca mice irradiated with 4 Gy gamma rays 24 h previously, but not immediately postirradiation, are able to induce DNA damage and apoptosis in nonirradiated bone marrow cells. The signaling mechanism involves FasL, TNF-alpha, nitric oxide and superoxide and macrophages are implicated as a source of damaging signals. Such delayed bystander-type damage demonstrates the importance of studying tissue responses subsequent to the radiation exposure as well as effects at the time of irradiation when considering the mechanisms underlying the consequences of radiation exposures.",
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    Burr, KL, Robinson, JI, Rastogi, S, Boylan, MT, Coates, PJ, Lorimore, SA & Wright, EG 2010, 'Radiation-induced delayed bystander-type effects mediated by hemopoietic cells', Radiation Research, vol. 173, no. 6, pp. 760-8. https://doi.org/10.1667/RR1937.1

    Radiation-induced delayed bystander-type effects mediated by hemopoietic cells. / Burr, Karen L.; Robinson, Joanne I.; Rastogi, Shubhra; Boylan, Michael T.; Coates, Philip J.; Lorimore, Sally A.; Wright, Eric G.

    In: Radiation Research, Vol. 173, No. 6, 2010, p. 760-8.

    Research output: Contribution to journalArticle

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    AB - Genetic lesions and cell death associated with exposure to ionizing radiation have generally been attributed to DNA damage arising as a consequence of deposition of energy in the cell nucleus. However, reports of radiation-induced bystander effects, in which DNA damage is produced in nonirradiated cells as a consequence of communication with irradiated cells, indicate additional mechanisms. At present, most information has been obtained using in vitro systems, and the in vivo significance of bystander factors is not clear. In this study we show that signals generated in vivo in the bone marrow of CBA/Ca mice irradiated with 4 Gy gamma rays 24 h previously, but not immediately postirradiation, are able to induce DNA damage and apoptosis in nonirradiated bone marrow cells. The signaling mechanism involves FasL, TNF-alpha, nitric oxide and superoxide and macrophages are implicated as a source of damaging signals. Such delayed bystander-type damage demonstrates the importance of studying tissue responses subsequent to the radiation exposure as well as effects at the time of irradiation when considering the mechanisms underlying the consequences of radiation exposures.

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    Burr KL, Robinson JI, Rastogi S, Boylan MT, Coates PJ, Lorimore SA et al. Radiation-induced delayed bystander-type effects mediated by hemopoietic cells. Radiation Research. 2010;173(6):760-8. https://doi.org/10.1667/RR1937.1