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NEUTRON DOSE PROTRACTION EFFECT ON TRANSFORMATION

中子剂量对转变的延长效应

基本信息

批准号：
3184378
负责人：
COLIN K HILL
金额：
$ 22.49万
依托单位：
UNIVERSITY OF SOUTHERN CALIFORNIA
依托单位国家：
美国
项目类别：
财政年份：
1985
资助国家：
美国
起止时间：
1985-11-01 至 1994-08-31
项目状态：
已结题

项目摘要

The long term objective of this application is to define and begin to search for an understanding of the enhanced effects that exposures to neutrons at low doses and doses rates cause on such endpoints as neoplastic transformation and mutation. In particular, the study will define at the cell level the energy dependence of this phenomenon both to gain more knowledge of the biophysical limitations determining the effects and to determine if the risks to humans exposed are confined to those occupationally exposed to fission neutrons or to a wider spectrum of people who may be exposed to neutons and other high LET radiations of various energies. In order to do this, the specific aims of the project are: 1. To define more clearly the energy dependence of enhanced carcinogeneic effects at low doses with protracted exposures to neutrons. 2. To make a molecular analysis of DNA from mutant clones produced by exposing cells to neutrons of various energies. 3. To define the role of repair of strand breaks and the significance of unrepaired breaks produced by exposure of cells to neutrons to various energies. 4. To test the hypothesis that low dose rate neutrons have "promoter-like" properties. 5. To test the hypothesis that a form of error-prone repair may be involved in both the production and the expression of lesions that cause the enhanced effects. Using neutrons produced at the UCLA cyclotron from protons on Beryllium at 46, 30, 20, and 12 MeV, the following major endpoints will be measured after rodent and human cells are exposed to acute and/or protracted exposures: Neoplastic transformation in C3H10T1/2 cells, mutation at the HGPRT and TK loci in V79, transformed human P3 and/or normal human IMR- 91 cells, DNA single and double strand break production, its repair and fidelity of the repair and finally restriction fragment analysis of DNA from mutant clones to determine what are the deletion types and patterns.

本申请的长期目标是定义并开始来寻求对增强效应的理解，在低剂量和剂量率下的中子照射会导致终点为肿瘤转化和突变。在特别是，该研究将在细胞水平上定义能量对这种现象的依赖性既要获得更多的知识，决定影响的生物物理限制，确定人类暴露的风险是否仅限于那些职业性地暴露于裂变中子或更宽的谱可能暴露于中子和其他高LET的人各种能量的辐射。为此，具体该项目的目标是： 1. 为了更清楚地界定增强型生物燃料的能源依赖性，长期接触低剂量的致癌作用中子 2. 对突变克隆的DNA进行分子分析通过将细胞暴露于不同能量的中子中而产生。 3. 为了明确链断裂修复的作用，细胞暴露于中子到各种能量。 4. 为了验证低剂量率中子 “启动子样”性质。 5. 为了验证一种假设，即一种易出错的修复形式可能参与病变的产生和表达导致增强效应的原因。利用加州大学洛杉矶分校回旋加速器从质子产生的中子，在46，30，20和12 MeV的Berg，以下主要将在啮齿动物和人类细胞急性和/或长期接触：肿瘤 C3 H10 T1/2细胞中的转化、HGPRT突变和 V79、转化的人P3和/或正常人IMR中的TK基因座 91细胞，DNA单双链断裂产生，修复以及修复的精确性，最后是限制性片段分析从突变克隆DNA，以确定什么是删除类型和模式。