量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果(学会誌発表論文、学会発表、研究開発報告書、特許等)を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum and Radiological Science and Technology.
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Existence of radioadaptive response (RAR) was reported in varied biosystems. RAR is capable of reducing genotoxicity, cell transformation, mutation and carcinogenesis but the underlying mechanisms remain fragmented. The first RAR mouse model called “Yonezawa Effect” was established by Yonezawa and colleagues using low LET X-rays as both the priming and the challenge doses, and rescue of bone marrow death as the endpoint. In a series of investigations, we further demonstrated that existence of RAR using different types of ionizing radiation (IR) including high LET heavy ions; increase in the hematopoietic stem cells/hematopoietic progenitor cells (HSCs/HPCs) measured as endogenous colony forming units-spleen under RAR; and reduction of delayed homologous recombination (HR) in the nucleated cells in hematopoietic tissues (bone marrow and spleen). These findings suggest that RAR in mice induced by different types of IR would share a common underlying mechanism: the priming IR-induced resistance in the blood forming tissues, leading to a protective effect on the HSCs/HPCs and rescuing the animals from bone marrow death. On the other hand, reduction of delayed HR may be at least a part of the mechanisms underlying decreased carcinogenesis by RAR. These findings provide a new insight into the mechanistic study on RAR in vivo and suggest that application of RAR would contribute to a more rigorous and scientifically-grounded system of radiation protection.