Research and development of transgenic mouse for biological effect assesment of tritium
Research and development of transgenic mouse for biological effect assesment of tritium
批准号:
07558074
负责人:
KOMATSU Kenshi
金额:
$4.42万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1995
资助国家:
日本
项目状态:
已结题
起止时间:
1995 至 1996
中文摘要
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英文摘要
We applied the transgenic mouse for analysis of tritium beta rays-induced mutation. In prsent study. Ingeno mouse developped by Gossen was used to detect the deleted mutation by ionizing radiation. Although coventional transgenic mouse is not appropriate for study of radiation-induced mutation, Ingeno mouse is expected to be useful for such mutations by transfection of 40 copy LacZ gene with plasmid pUR228. However, there are several problems to overcome for practical utilization. Among them, we successfully improved here technical problems, such us rescure methods of mutated lacZ gene into E.Coli and also positive selection of mutated gene by p-gal, indicating the availability for tritium biological study. This is confirmed by the evidences that RBE of neutron and carbon beam assayd by using Ingeno mouse is in agreement with that reported previously by others. These results also suggest that RBE of tritium is approximately 2. However, Ingeno mouse was appeared to be less radiation sensitive, i.e., 3.22*10^<-4>,5.37*10^<-4>,4.68*10^<-4> of mutation freguency at 0.5Gy, 10Gy of irradiation dose, respectively, and show necessity of further improvement as to radiation sensitivity. Using the hamster hybrid cells containing a single human X chromosome, we clarified the reason for less sensitivity of Ingeno mouse, suggesting the possibility of develop for radiation sensitive new transgenic mouse, which is 100-fold more sensitive than conventional assay. Consequently, our results demonstrated the usefulness of trasgenic mouse for future tritium biological study, such as specificity of DNA damage or hormesis response by tritium.
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小松賢志: "トリチウム生物影響「晩発効果・発がん」,(核融合,池上英雄他編)" 名古屋大学出版会,名古屋, 981(756-760) (1996)
Kenji Komatsu:“氚生物效应‘晚期效应/致癌’,(核聚变,由 Hideo Ikegami 等人编辑)” 名古屋大学出版社,名古屋,981(756-760)(1996)
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H.Kimura,K.Komatsu,et.al.: "The scid mutation on does not affect slowly repairing potentially lethal damage that is sensitive to 0.23 M NaCl." J.Rad.Res.37. 247-255 (1996)
H.Kimura、K.Komatsu 等人:“scid 突变不会影响对 0.23 M NaCl 敏感的潜在致命损伤的缓慢修复。”
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H.Tauchi,K.Komatsu,et.al.: "Accumulation of cells at G_2/M stage by low dose-rate irradiation renders the cell population more susceptible to the subsequent induction of 6-thioguanine-resistant mutations by _<252>Cf fission neutrons." J.Rad.Res.37. 49-57
H.Tauchi、K.Komatsu 等人:“通过低剂量率照射,G_2/M 期细胞的积累使细胞群更容易受到 _<252> 随后诱导的 6-硫鸟嘌呤抗性突变的影响。
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T.Honda,K.Komatsu,et.al.: "Spontaneous immortalization of cultured skin fibroblasts obtained from a high-dose atomic bomb survivor." Mutat.Res.354. 15-26 (1996)
T.Honda、K.Komatsu 等人:“从高剂量原子弹幸存者获得的培养皮肤成纤维细胞的自发永生化。”
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共 8 条
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Induction of DNA double strand break by environmental genotoxic and carcinogenic agents
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FUNCTIONAL ANALYSIS OF CANCER-SUSCEPTIBIE GENE, NBS1
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Origin of radiation-induced genomic instability
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Cancersusceptibility disease Nijmegen Breakage Syndrome and the function of underlying gene.
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批准号:12213087
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财政年份:2000
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Study on underlying gene of Nijmegen Breakage Syndrome
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财政年份:1998
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依托单位:
Development of (a human X-chromosome * hamster) hybrid cell assay system, which is sensitive to tritium exposure.
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批准号:09558064
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项目类别:Grant-in-Aid for Scientific Research (B)
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财政年份:1997
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依托单位:
Molecular study on Nijmegen breakage sybdrome
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资助金额:$3.52万
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财政年份:1996
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依托单位:
Multi-functions of DNA-dependent protein kinase (DNA-PK) and the association of radiation sensitivity
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财政年份:1996
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依托单位:
Study on biological effectiveness of organic bound tritium by using DNA deficient cells.
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财政年份:1994
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The Mechanism of Hyper-radiosensitivity Expressed in Ataxia telangiectasia Disease.
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财政年份:1990
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Modulating Effect of Protein Kinase C Activator on Radiation-Induced Transformation
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负责人:KOMATSU Kenshi
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