Bulletin of Experimental Biology and Medicine

, Volume 124, Issue 1, pp 668–671 | Cite as

λ-Radiation-induced irreparable damage to DNA of HeLa cells

  • V. A. Struchkov
  • N. I. Demidova
  • N. B. Strazhevskaya
Biophysics and Biochemistry


Exposure of HeLa cells to λ-radiation at 0.1 Gy and then at 5 Gy reduces their ability to repair double-strand DNA breaks to a greater extent than irradiation with a single dose of 5 Gy. Modifying effects of 0.1 Gy on double-strand DNA breaks and on cell survival are observed after irradiation during logarithmic but not stationary phase of growth. Primary λ-induced irreparable double-strand breaks correlates with cell survival regardless the irradiation regime. It is suggested that such a damage is primarily responsible for reproductive death of HeLa cells.

Key Words

λ-radiation DNA damage HeLa cells 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Kh. Abel', G. Ertsgreber, and K. Langrok,Radiobiologiya,23, No. 4, 435–438 (1983).Google Scholar
  2. 2.
    N. Ya. Gil'yano, A. M. Ikhtiar, and O. V. Malinovskii,Radiobilogiya,33, No. 2, 197–204 (1993).Google Scholar
  3. 3.
    N. I. Demidova, “Growth characteristics of tumor cellsin vitro after low-dose irradiation,” Author's Synopsis of Dissertation [in Russian], Moscow. (1991).Google Scholar
  4. 4.
    G. S. Kalendo, “Augmentation of damaging effects from ionizing radiation by factors inducing short-term activation of cellular metabolism,” Author's Synopsis of Doct. Biol. Sci. Dissertation [in Russian], Moscow (1977).Google Scholar
  5. 5.
    G. S. Kalendo,Early Cell Responses to Ionizing Radiation and Their Role in Protection and Sensitization, [in Russian], Moscow (1982).Google Scholar
  6. 6.
    I. I. Pelevina, G. G. Afanas'ev, and V. Ya. Gotlib,Cellular Factors in Responses of Tumors to Radiation and Chemotherapeutic Agents [in Russian], Moscow (1978).Google Scholar
  7. 7.
    V. A. Struchkov and N. B. Strazhevskaya,Biokhimiya,58, No. 8, 1154–1175 (1993).Google Scholar
  8. 8.
    N. I. S'yakste, G. S. Kalendo, A. V. Likhtenshtein,et al., Byull. Eksp. Biol. Med.,94, No. 12, 38–40 (1982).Google Scholar
  9. 9.
    E. Ben Hur and M. M. Elkind,Radiat. Res.,59, No. 2, 484–492 (1974).PubMedGoogle Scholar
  10. 10.
    P. R. Cook and I. A. Brazell,J. Cell Sci.,22, No. 3, 287–302 (1976).PubMedGoogle Scholar
  11. 11.
    M. M. Elkind, H. Utsumi, T. Kosaka,et al., J. Cell. Biochem. Suppl., No. 12A 286 (1988).Google Scholar
  12. 12.
    P. Kanster, K. J. Leister, L. D. Temei,et al., Biochem. Biophys. Res. Commun.,118, No. 3, 392–399 (1984).CrossRefGoogle Scholar
  13. 13.
    T. T. Puck, P. J. Marcus, and S. J. Cieciura,J. Exp. Med.,103, No. 2, 273–284 (1956).PubMedCrossRefGoogle Scholar
  14. 14.
    I. R. Radford,Int. J. Radiat. Biol.,49, No. 4, 611–620 (1986).CrossRefGoogle Scholar
  15. 15.
    K. Sakai and S. Okada,Radiat. Res.,98, No. 3, 479–490 (1984).PubMedGoogle Scholar

Copyright information

© Plenum Publishing Corporation 1998

Authors and Affiliations

  • V. A. Struchkov
    • 1
  • N. I. Demidova
    • 1
  • N. B. Strazhevskaya
    • 1
  1. 1.Laboratory of Cellular Metabolism, Institute of Experimental Diagnosis and Therapy of Tumors, Oncology Research CenterRussian Academy of Medical SciencesMoscow

Personalised recommendations