Annual report on the environmental radiation monitoring around the Tokai Reprocessing Plant FY2022

Kokubun, Yuji; Nakada, Akira; Seya, Natsumi; Koike, Yuko; Nemoto, Masashi; Tobita, Keiji; Yamada, Ryohei*; Uchiyama, Rei; Yamashita, Daichi; Nagai, Shinji; et al.

JAEA-Review 2023-046, 164 Pages, 2024/03

JAEA-Review-2023-046.pdf:4.2MB

The Nuclear Fuel Cycle Engineering Laboratories conducts environmental radiation monitoring around the reprocessing plant in accordance with the "Safety Regulations for Reprocessing Plant of JAEA, Part IV: Environmental Monitoring". This report summarizes the results of environmental radiation monitoring conducted during the period from April 2022 to March 2023 and the results of dose calculations for the surrounding public due to the release of radioactive materials into the atmosphere and ocean. In the results of the above environmental radiation monitoring, many items were affected by radioactive materials emitted from the accident at the Fukushima Daiichi Nuclear Power Plant of Tokyo Electric Power Company, Incorporated (changed to Tokyo Electric Power Company Holdings, Inc. on April 1, 2016), which occurred in March 2011. Also included as appendices are an overview of the environmental monitoring plan, an overview of measurement methods, measurement results and their changes over time, meteorological statistics results, radioactive waste release status, and an evaluation of the data which deviated of the normal range.

Experimental determination of the topological phase diagram in Cerium monopnictides

Kuroda, Kenta*; Ochi, Masayuki*; Suzuki, Hiroyuki*; Hirayama, Motoaki*; Nakayama, Mitsuhiro*; Noguchi, Ryo*; Bareille, C.*; Akebi, Shuntaro*; Kunisada, So*; Muro, Takayuki*; et al.

Physical Review Letters, 120(8), p.086402_1 - 086402_6, 2018/02

https://doi.org/10.1103/PhysRevLett.120.086402

Induction of DNA DSB and its rejoining in clamped and non-clamped tumours after exposure to carbon ion beams in comparison to X-rays

Hirayama, Ryoichi*; Uzawa, Akiko*; Matsumoto, Yoshitaka*; Noguchi, Miho; Kase, Yuki*; Takase, Nobuhiro*; Ito, Atsushi*; Koike, Sachiko*; Ando, Koichi*; Okayasu, Ryuichi*; et al.

Radiation Protection Dosimetry, 143(2-4), p.508 - 512, 2011/02

https://doi.org/10.1093/rpd/ncq478

We studied double-strand breaks (DSB) induction and rejoining in clamped and non-clamped transplanted tumours in mice leg after exposure to 80 keV/m carbon ions and X-rays. The yields of DSB in the tumours were analysed by a static-field gel electrophoresis. The OER of DSB after X-rays was 1.68, and this value was not changed after 1 h rejoining time (1.40). These damages in oxygenated conditions were rejoined 60-70% within 1 h in situ. No difference was found between the exposure to X-rays and carbon ions for the induction and rejoining of DSB. Thus, the values of OER and rejoined fraction after exposure to carbon ions were similar to those after X-rays, and the calculated relative biological effectivenesses of carbon ion were around 1 under both oxygen conditions. The yields of DSB in vivo depend on exposure doses, oxygen conditions and rejoining time, but not on the types of radiation quality.

Enhanced radiation-induced cell killing by Herbimycin A pre-treatment

Noguchi, Miho; Hirayama, Ryoichi*; Druzhinin, S.*; Okayasu, Ryuichi*

Radiation Physics and Chemistry, 78(12), p.1184 - 1187, 2009/12

https://doi.org/10.1016/j.radphyschem.2009.07.008

Herbimycin A (HA), as in Geldanamycin, binds to conserved pockets of heat shock protein 90 (Hsp90) and inhibits its chaperone functions. Hsp90 plays an integral role in cancer cell growth and survival, because it maintains the stability of several key proteins by its chaperone's activity. It is known that some of the proteins associated with radiation responses are functionally stabilized by Hsp90. In this study, we investigated the effect of HA on radiosensitivity in human cancer cells and the mechanism related to the sensitization. In order to gain a mechanistic insight of this sensitization, we examined repair of DNA double strand breaks (DSBs) in irradiated human cancer cells pre-treated with HA, as unrepaired DSBs are thought to be the main cause of radiation-induced cell death. Cellular radiosensitivity was determined by clonogenic assay, and the DSB rejoining kinetics was examined by constant field gel electrophoresis. SQ-5, a lung squamous carcinoma cell line, showed synergistic increase in radiosensitivity when cells were pre-treated with HA. In addition, HA significantly inhibited repair of radiation induced DSBs. These results suggest that the combination of HA and ionizing radiation may be a useful therapeutic strategy for treating certain cancer cells.

Contributions of direct and indirect actions in cell killing by high-LET radiations

Hirayama, Ryoichi*; Ito, Atsushi*; Tomita, Masanori*; Tsukada, Teruyo*; Yatagai, Fumio*; Noguchi, Miho; Matsumoto, Yoshitaka*; Kase, Yuki*; Ando, Koichi*; Okayasu, Ryuichi*; et al.

Radiation Research, 171(2), p.212 - 218, 2009/02

https://doi.org/10.1667/RR1490.1

The biological effects of radiation originate principally in damages to DNA. DNA damages by X-rays as well as heavy ions are induced by a combination of direct and indirect actions. The contribution of indirect action in cell killing can be estimated from the maximum degree of protection by dimethylsulfoxide (DMSO), which suppresses indirect action without affecting direct action. Exponentially growing Chinese hamster V79 cells were exposed to high-LET radiations of 20 to 2106 keV/m in the presence or absence of DMSO and their survival was determined using a colony formation assay. The contribution of indirect action to cell killing decreased with increasing LET. However, the contribution did not reach zero even at very high LETs and was estimated to be 32% at an LET of 2106 keV/m. Therefore, even though the radiochemically estimated G value of OH radicals was nearly zero at an LET of 1000 keV/m, indirect action by OH radicals contributed to a substantial fraction of the biological effects of high-LET radiations. The RBE determined at a survival level of 10% increased with LET, reaching a maximum value of 2.88 at 200 keV/m, and decreased thereafter. When the RBE was estimated separately for direct action (RBE(D)) and indirect action (RBE(I)); both exhibited an LET dependence similar to that of the RBE, peaking at 200 keV/m. However, the peak value was much higher for RBE(D) (5.99) than RBE(I) (1.89). Thus direct action contributes more to the high RBE of high-LET radiations than indirect action does.

Development of irradiation technology with temperature control

Kagota, Eiichi; Noguchi, Koichi; Kitamura, Ryoichi; Abe, Kazuyuki

no journal, , 

no abstracts in English

The Heat shock protein 90 inhibitor 17-AAG may cause DNA double strand break repair inhibition

Noguchi, Miho; Yu, D.*; Hirayama, Ryoichi*; Kubota, Nobuo*; Okayasu, Ryuichi*

no journal, , 

The aim of this study is to evaluate the radiosensitization of Hsp90 inhibitor 17-Allylamino-17-demethoxygeldanamycin (17AAG), specifically the effect of 17AAG on the DNA DSB repair machinery. Our constant field gel electrophoresis studies indicated that pretreatment with 17AAG for 24 hours inhibited radiation induced DSB repair in two cancer cell lines (DU145 and SQ-5). The treatment of 17AAG alone leads to the reduction of Rad51 protein expression by western blotting, and the combined treatment with X-irradiation caused a delay in the formation of nuclear Rad51 foci by immuno-staining. These results suggest that 17AAG affects the key protein(s) for HRR, resulting in the radiosensitization of tumor cells. Our data show for the first time that 17AAG is a DNA DSB repair inhibitor, predominantly affecting the homologous recombination pathway.

Radiosensitization by inhibition of homologous recombination repair combined with high LET heavy ion irradiation

Okayasu, Ryuichi*; Hirakawa, Hirokazu*; Noguchi, Miho; Yu, D.*; Takahashi, Momoko; Hirayama, Ryoichi*; Fujimori, Akira*

no journal, , 

17AAG, an Hsp90 inhibitor was shown to radiosensitize certain human tumor cells exposed to X-rays, while this sensitization was not clearly observed in normal human cells. The mechanism of this was suggested to come from inhibition of DNA double strand break (DSB) repair, particularly impairment of homologous recombination repair (HRR) pathway by this drug (Noguchi et al 2006). Key proteins associated with HRR seem to be affected by this inhibitor. To our surprise, tumor radiosensitization with 17AAG was also observed in cells exposed to high LET carbon ions (70 kev/um). Independently we also found that knockdown of BRCA2, a key HRR protein significantly radiosensitized human tumor cells. These results indicate that there seem to be a radio-sensitization mechanism associated with the combination of HRR inhibition and high LET radiation, and this may occur particularly in S-phase cells. Furthermore, we also used mouse xenograft model to examine the combined effect of 17AAG and high LET carbon irradiation. For this purpose, SQ5 human lung tumor cells were implanted on the leg of nude mice and the tumor growth was observed in the combined treatment as compared with radiation or drug treatment alone. Our preliminary results indicate that tumor growth was more inhibited in the 17AAG and carbon irradiation than carbon or 17AAG treatment alone. These data suggest that an effective tumor control might be obtained by combining an HRR inhibitor with high LET carbon irradiation.

Rejoining of DNA double-strand breaks in hypoxic cells following irradiation by X-rays and heavy ions

Hirayama, Ryoichi*; Matsumoto, Yoshitaka*; Noguchi, Miho; Uzawa, Akiko*; Koda, Kana*; Furusawa, Yoshiya*

no journal, , 

The presence or absence of molecular oxygen dramatically influences the biological effect of low LET radiations. To produce oxygen effect, molecular oxygen must be present during the radiation exposure or at least during the lifetime of the free radicals generated by the radiation. Little study has been done to actually investigate the influence of oxygen after the radiation exposure. The present study was undertaken in order to explore the rejoining activity of DNA-DSB induced by anaerobic X-ray or carbon ion (80 keV/m) irradiations under oxic and hypoxic holdings (37 C). DNA-DSB in CHO cells were analyzed by a static-field gel electrophoresis. The kinetics of the rejoining could be described by a sum of fast and slow components. The slow component of DNA-DSB induced by X-ray under oxic incubation was faster than that under hypoxic incubation. Furthermore, the percentages of non-reparable DNA damage were 5% and 20% under oxic and hypoxic incubation conditions, respectively. However, no difference between oxic and hypoxic incubation conditions was found for carbon ion irradiation. There results indicate that molecular oxygen influences the rejoining of DNA-DSB after low LET radiation exposure.

RBS study of behavior of Cu diffusion in -FeSi

Noguchi, Masaya*; Mizuki, Tatsuya*; Kawakubo, Yuki*; Hirata, Tomoaki*; Kagawa, Seiya*; Nagatsuyu, Tomohiro*; Iwamoto, Ryotaro*; Shibahara, Kohei*; Narumi, Kazumasa; Maeda, Yoshihito

no journal, , 

no abstracts in English

Absorption and translocation of radioactive cesium in Cypress planted trees

Hirai, Keizo*; Komatsu, Masafumi*; Akama, Akio*; Noguchi, Ryotaro*; Nagakura, Junko*; Ohashi, Shinta*; Saito, Tetsu*; Kawasaki, Tatsuro*; Yazaki, Kenichi*; Ikeda, Shigeto*; et al.

no journal, , 

no abstracts in English