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Matsuya, Yusuke; Satou, Yukihiko; Hamada, Nobuyuki*; Date, Hiroyuki*; Ishikawa, Masayori*; Sato, Tatsuhiko
no journal, ,
Following the incident at the Fukushima Dai-ichi Nuclear Power Station (F1NPS) in 2011, insoluble radioactive microparticles (so called Cs-bearing particle) have been found in the land area around F1NPS. The energy deposition by such a particle is localized mainly by 
-rays in cells close to a Cs-bearing particle. There is no literature on the biological effects after such particle exposures. Here, we investigated DNA lesions after long-term exposure to a Cs-bearing particle in comparison with a uniform exposure to Cs-137 
-rays. From dose calculation by a Monte Carlo simulation and the experiments in vitro, the several DNA lesions in the cells distal to the particle and the less lesions induction in the cells close to the particle were observed in the comparison with the uniform exposure. The increase of lesions in number was suppressed by 1% DMSO, suggesting the involvement of reactive oxygen species. Considering the small organ dose, the conventional radiation risk assessment is adequate. This study is the first to quantify the relationship between absorbed dose-rate and nuclear DNA damage under long-term heterogeneous exposure to a Cs-bearing particle.
Takahashi, Rei*; Saga, Ryo*; Matsuya, Yusuke; Hasegawa, Kazuki*; Fukui, Roman*; Hosokawa, Yoichiro*
no journal, ,
Inflammatory responses after irradiation induce antioxidant activity, leading to radioresistance in cancer cells. In our previous study, it was found that a hyaluronan synthesis inhibitor (4-MU) can suppress inflammatory responses, however the underlying mechanisms are still unknown. In this study, we aimed to clarify the radiosensitization mechanism induced by 4-MU in the application of cell-killing models. In terms of in vitro experiments, cultured human fibrosarcoma cells were exposed to X-rays in presence of 100 
M 4-MU and scavenger of intercellular signalling (1% DMSO, 40 M c-PTIO), and we measured the relation between dose and cell viability by means of colony assay. The experimental results were also interpreted by using integrated cell-killing model which has been developed so as to consider non-targeted effects. From the experiments, it was found that a combination of 4-MU treatment and irradiation significantly reduced the cell survival. This reduced viability was suppressed in the presence of DMSO or c-TPIO. Meanwhile, the model analysis showed such an increase of cell-killing is predominantly attributed by non-targeted effects. These results suggest that the radiosensetization promoted by 4-MU treatment is predominantly attributed to the accumulation in non-targeted effects.
Kanzaki, Norie; Shimada, Mikio*; Yanagihara, Hiromi*
no journal, ,
After ionizing radiation exposure, several types of DNA damage occur in mammalian cells. Several studies have been reported that the mutation type depends on the radiation type and the cell type. Thus, it is important to characterize the type of mutation caused by irradiation for understanding of the biological effects of radiation. This study is a foundational investigation of construction of data analysis method dedicated to characteristics extraction of mutations. Two datasets were hypothetically made by reference to previous researches. The data was composed of eight items, namely two types of transition, four types of transversion, insertion, and deletion. The datasets were first analyzed by Self-Organizing Maps. We categorized and predicted the characteristics of mutations. This result was compared with those of other multivariate analysis methods. The data with similar mutation patterns was closely located on the output map, indicating the variation of mutations given by different radiation types.
Oka, Toshitaka; Takahashi, Atsushi*; Koarai, Kazuma; Ono, Takumi*; Tamaki, Hiroaki*; Kino, Yasushi*; Sekine, Tsutomu*; Shimizu, Yoshinaka*; Chiba, Mirei*; Suzuki, Toshihiko*; et al.
no journal, ,
Releases of the radioactive materials from the Fukushima Daiichi Nuclear Power Plant accident result in an ionization exposure to people and animals, the precise dosimetry is required. To estimate the external dose due to the accident, we utilize electron spin resonance (ESR) spectroscopy which is a powerful tool for the dosimetry of external dose. The detection limit of this technique was 146 mGy, so that we have to improve the detection limit for the precise dosimetry. In this work, we developed a novel enamel-dentine separation technique and improved the detection limit down to 43 mGy, and estimated the external dose for Japanese macaque and Procyon lotor collected in Fukushima prefecture.
Kataoka, Takahiro*; Kanzaki, Norie; Sakoda, Akihiro; Ishida, Tsuyoshi; Tanaka, Hiroshi; Hanamoto, Katsumi*; Terato, Hiroaki*; Mitsunobu, Fumihiro*; Yamaoka, Kiyonori*
no journal, ,
We have reported that radon inhalation inhibits oxidative induced damages in some mouse organs due to activation of antioxidant functions. These activations are probably induced by reactive oxygen species following radon inhalation. In this study, we assayed the production of hydrogen peroxide and antioxidant associated substances in brain, lung, heart, liver, stomach, pancreas, kidney, small intestine, and colon in mouse after radon inhalation (1,000 or 10,000 Bq/m
for 24 hours). Results showed that radon inhalation significantly decreased LPO levels in liver (1,000 Bq/m and 10,000 Bq/m) and heart (1,000 Bq/m), suggesting that radon inhalation inhibits oxidative stress. However, On the other hand, radon inhalation at a concentration of 10,000 Bq/m significantly increased the levels of LPO and hydrogen peroxide in lungs only. These findings suggested that radon inhalation at high concentration does not induce oxidative stress in other organs except lung.