AT Cells Show Dissimilar Hypersensitivity to Heavy-Ion and X-rays Irradiation

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  • KITAJIMA Shoichiro
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute Department of Oral and Maxillofacial Surgery, School of Dentistry, Aichi-Gakuin University
  • NAKAMURA Hideaki
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute Department of Mechanism of Aging, National Institute for Longevity Sciences
  • ADACHI Makoto
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute Department of Oral and Maxillofacial Surgery, Yokohama City University Graduate School of Medicine
  • IJICHI Kei
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute Department of Otolaryngology-Head and Neck Surgery, Nagoya City University Graduate School of Medical Sciences
  • YASUI Yoshihiro
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute
  • SAITO Noriko
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute
  • SUZUKI Masao
    Heavy-ion Radiobiology Research Group, National Institute Radiological Sciences
  • KURITA Kenichi
    Department of Oral and Maxillofacial Surgery, School of Dentistry, Aichi-Gakuin University
  • ISHIZAKI Kanji
    Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute

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Ataxia telangiectasia (AT) cells, with their defective double-strand break (DSB) repair processes, exhibit high sensitivity to low-LET radiation such as X-rays irradiation and gamma beams. Since heavy ion beam treatment for cancer is becoming increasingly common in Japan and elsewhere, it is important to also determine their sensitivity to high-LET radiation. For this purpose we irradiated AT and normal human cells immortalized with the human telomerase gene using high- (24–60 keV/μm carbon and 200 keV/μm iron ions) or low-LET (X-rays) radiation in non-proliferative conditions. In normal cells the RBE (relative biological effectiveness) of carbon and iron ions increased from 1.19 to 1.81 in proportion to LET. In contrast, their RBE in AT cells increased from 1.32 at 24 keV/μm to 1.59 at 40 keV/μm, and exhibited a plateau at over 40 keV/μm. In normal cells most γ-H2AX foci induced by both carbon- and iron-ion beams had disappeared at 40 h. In AT cells, however, a significant number of γ-H2AX foci were still observed at 40 h. The RBEs found in the AT cells after heavy-ion irradiation were consistent with the effects predicted from the presence of non-homologous end joining defects. The DSBs remaining after heavy-ion irradiation suggested defects in the AT cells' DSB repair ability.

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