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Development and analysis of human organ/tissue damage by fission radionuclides

裂变放射性核素对人体器官/组织损伤的发展和分析

基本信息

批准号：
16201013
负责人：
NOMURA Taisei
金额：
$ 31.53万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (A)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16201013/
关键词：
fission radionuclides mouse with human tissues organ and tissue damage mutation in human tissues change in gene expression functional damage severe combined immuno-deficiency radioactive iodine 放射線ヨード放射線ヒト臓器・組織障害ヒト甲状腺ホルモン分泌能

项目摘要

1.Production of SCID mice with human organs and tissues (thyroid, bone marrow cells, lung, embryonic tissues)2.Effects of fission radionuclides on human tissues.(1) Dose rate of fission neutron and γ-rays from UTR-KINKI (1W, max 10^7n/cm^2-.sec) in the mouse body was measured; 0.2 Gy neutron and 0.2 Gy γ-rays per hour.(2) Weekly doses of 0.2 Gy of neutron were given 6 times to the transplated human thyroid tissues from Graves' disease patients and also 4 times to the human lung tissues grown from embryonic lung at 11 weeks. No p53, K-ras, c-kit, β-catenin, RET, bak, BRAF mutations were detected by these doses in the thyroid and lung tissues, while large doses (11-33 Gy) of ^<137>Cs γ-rays induced 8 mutations (6 p53 and 2 c-kit) in 20 irradiated human thyroid tissues. GeneChip analyses (8500 genes) revealed 4 fold increases or decreases of gene expression in 59.7 genes of thyroid tissues and 18.5 genes of lung tissues 1 week after exposure to neutrons (0.2 Gy × 4).3.Effects of ^<131>I : 0.5 MBq/mouse of ^<131>I was given weekly to SCID mice with human thyroid tissues. Six mutations were induced in 18 thyroid tissues exposed for more than 37 weeks, but only 2 mutations in 24 tissues for less than 36 weeks; 7 p53 and 1 β-catenin mutations. Single dose of 0.06-0.5 MBq/mouse of ^<131>I induced 4 fold increases or decreases in gene expression of 25-51.5 genes, suggesting very strong effects of radioiodine.4.In the liquidators exposed to radionuclides from the catastrophe of Chernobyl nuclear plant, abnormal overexpression of WT1 gene was observed and 2 became leukemia. Microsatellite mutation was also examined in the children of liquidators exposed to radionuclides.5.^<137>Cs γ-ray induced congenital malformation and leukemia were inhibited significantly by active hexose correlated compound.

1.用人体器官和组织（甲状腺、骨髓细胞、肺、胚胎组织）生产SCID小鼠2.裂变放射性核素对人体组织的影响。(1)测量了UTR-KINKI裂变中子和γ射线（1 W，最大10^7 n/cm ^2-.sec）在小鼠体内的剂量率;每小时0.2戈伊和0.2戈伊射线。(2)对移植的Graves病患者甲状腺组织和11周人胚肺组织分别给予每周剂量为0.2戈伊的中子照射6次和4次。大剂量（11-33戈伊）~（60）Cs γ射线照射20例甲状腺组织，未发现p53、K-ras、c-kit、β-catenin、RET、巴克、BRAF突变<137>。基因芯片分析（8500个基因）显示，在0.2戈伊× 4的中子照射后1周，甲状腺组织中有59.7个基因和肺组织中有18.5个基因的基因表达增加或减少了4倍<131><131>。在暴露超过37周的18个甲状腺组织中诱导了6个突变，但在暴露少于36周的24个组织中仅诱导了2个突变; 7个p53和1个β-catenin突变。0.06- 0.5MBq/只的单次剂量<131>的~（13）I可诱导25-51.5个基因表达增加或减少4倍，表明放射性碘具有很强的作用。4.在切尔诺贝利核电站事故放射性核素暴露的清理者中，观察到WT 1基因异常过表达，其中2例发生白血病。在暴露于放射性核素的清理者的子女中也检查了微卫星突变。<137>活性己糖相关化合物对Cs γ射线诱发的先天畸形和白血病有明显的抑制作用。

项目成果

期刊论文数量（124）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Critical role of RecA and RecF proteins in strand break rejoining and maintenance of fidelity of rejoining following γ-radiation-induced damage to pMTa4 DNA in E. coli

RecA 和 RecF 蛋白在大肠杆菌中 γ 辐射诱导的 pMTa4 DNA 损伤后链断裂重新连接和维持重新连接保真度中的关键作用

DOI：
发表时间：
2007
期刊：
International Journal of Radiation Biology
影响因子：
2.6
作者：
R. Sharan;H. Ryo;T. Nomura
通讯作者：
T. Nomura

P53, K-ras, β-catenin, c-Kit and bak Mutations in Chineses and Japanese lung cancer cases.

中国和日本肺癌病例中的 P53、K-ras、β-catenin、c-Kit 和 bak 突变。

DOI：
发表时间：
2006
期刊：
Indian J. Radiation Research 2
影响因子：
0
作者：
Shuo Xing;et al.
通讯作者：
et al.

Male-mediated Developmental Toxicity (Chapter 12. Transmissible Genetic Risk Causing Tumours in Mice and Humans)

雄性介导的发育毒性（第 12 章。导致小鼠和人类肿瘤的传染性遗传风险）

DOI：
发表时间：
2007
期刊：
Royal Society of Chemistry
影响因子：
0
作者：
Nomura;T.
通讯作者：
T.

Transgenerational transmission of radiation- and chemically induced tumors and congenital anomalies in mice: studies of their possible relationship to induced chromosomal and molecular changes

DOI：
10.1159/000077499
发表时间：
2004-01-01
期刊：
CYTOGENETIC AND GENOME RESEARCH
影响因子：
1.7
作者：
Nomura, T;Nakajima, H;Tanaka, H
通讯作者：
Tanaka, H

Th1-biased humoral immune responses against Wilms tumor gene WT1 product in the patients with hematopoietic malignancies.

造血系统恶性肿瘤患者针对肾母细胞瘤基因WT1产物的Th1偏向体液免疫反应。

DOI：
发表时间：
2005
期刊：
Leukemia 19
影响因子：
0
作者：
Wu F;Oka Y;Tsuboi A;Elisseeva O. A;Nakajima H;Fujiki F;Masuda T;Murakami M;Yoshihara S;Ikegame K;Hosen N;Kawakami M;Nakagawa M;Kubota T;Soma T;Yamagami T;Tsukaguchi M;Ogawa H;Oji Y;Hamaoka T;Kawase I;Sugiyama H.
通讯作者：
Sugiyama H.