An Alternative Mechanism for Radioprotection by Dimethyl Sulfoxide; Possible Facilitation of DNA Double-strand Break Repair

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  • KASHINO Genro
    Laboratory of Radiation Biology, Research Reactor Institute, Kyoto University
  • LIU Yong
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • SUZUKI Minoru
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • MASUNAGA Shin-ichiro
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • KINASHI Yuko
    Laboratory of Radiation Safety and Control, Research Reactor Institute, Kyoto University
  • ONO Koji
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • TANO Keizo
    Laboratory of Radiation Biology, Research Reactor Institute, Kyoto University
  • WATANABE Masami
    Laboratory of Radiation Biology, Research Reactor Institute, Kyoto University

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Abstract

The radioprotective effects of dimethyl sulfoxide (DMSO) have been known for many years, and the suppression of hydroxyl (OH) radicals induced by ionizing radiation has been thought to be the main cause of this effect. However, the DMSO concentration used was very high, and might be toxic, in earlier studies. In the present study, we administered a lower, non-toxic concentration (0.5%, i.e., 64 mM) of DMSO before irradiation and examined its radioprotective effects. Colony formation assay and micronucleus assay showed significant radioprotective effects in CHO, but not in xrs5, which is defective in the repair function of DNA double-strand breaks. The levels of phosphorylated H2AX and the formation of 53BP1 foci 15 minutes after irradiation, which might reflect initial DNA double-strand breaks, in DMSO-treated CHO cells were similar to those in non-treated cells, suggesting that the radioprotective effects were not attributable to the suppression of general indirect action in the lower concentration of DMSO. On the other hand, 2 hours after irradiation, the average number of 53BP1 foci, which might reflect residual DNA double-strand breaks, was significantly decreased in DMSO-treated CHO cells compared to non-treated cells. The results indicated that low concentration of DMSO exerts radioprotective effects through the facilitation of DNA double-strand break repair rather than through the suppression of indirect action.

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