Transgenerational Effects of Radiation and Chemicals in Mice and Humans
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概要
- 論文の詳細を見る
Parental exposure of mice to radiation and chemicals causes a variety of adverse effects (e.g., tumors, congenital malformations and embryonic deaths) in the progeny and the tumor-susceptibility phenotype is transmissible beyond the first post-radiation generation. The induced rates of tumors were 100-fold higher than those known for mouse specific locus mutations. There were clear strain differences in the types of naturally-occurring and induced tumors and most of the latter were malignant. Another important finding was that germ-line exposure elicited very weak tumorigenic responses, but caused persistent hypersensitivity in the offspring for the subsequent development of cancer by the postnatal environment. Activations of oncogenes, ras, mos, abl, etc. and mutations in tumor suppressor genes such as p53 were also detected in specific tumors in cancer-prone descendants. However, the majority of tumors observed in the progeny were those commonly observed in the strains that were used and oncogene activations were rarely observed in these tumors. It can be hypothesized that genetic instability modifies tumor occurrence in a transgenerational manner, but so far no links could be established between chromosomal and molecular changes and transmissible tumor risks. Our data are consistent with the hypothesis that cumulative changes in many normal but cancer-related genes affecting immunological, biochemical and physiological functions may slightly elevate the incidence of tumors or fasten the tumor development. This hypothesis is supported by our GeneChip analyses which showed suppression and/or over-expression of many such genes in the offspring of mice exposed to radiation. In humans, a higher risk of leukemia and birth defects has been reported in the children of fathers who had been exposed to radionuclides in the nuclear reprocessing plants and to diagnostic radiation. These findings have not been supported in the children of atomic bomb survivors in Hiroshima and Nagasaki, who were exposed to higher doses of atomic radiation. However, it will be important to follow the human subjects, especially for adult type cancers and chronic diseases throughout their lives to determine whether the mouse studies can predict human responses.
- 日本放射線影響学会の論文
著者
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野村 大成
医薬基盤研究所
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NOMURA Taisei
Department of Radiation Biology and Medical Genetics, Graduate School of Medicine, Osaka University
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Nomura Taisei
大阪大学 医学系研究科生体制御医学専攻遺伝医学
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Nomura T
Department Of Radiation Biology Osaka University Medical School
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Nomura Taisei
Dept. Radiat. Biol. Med. Gen. Grad. Sch. Med. Osaka Univ.
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Nomura Taisei
Department Of Radiation Biology And Medical Genetics Graduate School Of Medicine Osaka University
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Nomura Taisei
Dept. Of Radiat. Biol.
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Nomura Takaharu
Low Dose Radiation Research Center Central Research Institute Of Electric Power Industry
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Nanmori Takashi
Department Of Animal Science Graduate School Of Agricultural Science Kobe University
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- γ線照射装置の照射野の自動制御
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- 定量的発がん性試験法
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- Suppressive Effect of Low Dose Rate Chronic Irradiation on Carcinogenesis
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- ACKNOWLEDGEMENTS
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- Mitochondria-Targeted Superoxide Dismutase (SOD2) Regulates Radiation Resistance and Radiation Stress Response in HeLa Cells