CELL RADIATION RESPONSE AT LOW DOSE RATES

对于一般人群来说，生物活性剂的危害 在我们的环境中--或与卫生服务相关的--预计将 低剂量长期使用的结果。 的危害 主要关注是与细胞失活、突变 转化和改变的分化。 估计程度 风险，习惯上假设效果遵循线性或 “单次命中”剂量依赖性，其速率通常可从 从高剂量传递产生的效应外推到零剂量， 高剂量率。 与线性假设相关的是 隐含的假设，即效应的大小与 剂量输送速率。 这个假设来自传统的 目标理论的应用，即，一个单一的吸收事件 敏感的目标产生效果。 因此，次有效 事件未登记，因此，生化/生物过程 在曝光期间或曝光之间不能改变效果的程度。 然而，在这方面， 传统上应用的靶理论只是一种限制性的解决方案， 更一般的关系，根据该关系，如果仅 目标中的吸收事件的（剂量无关的）分数是 有效 因此，发生的生物化学/生物过程 在长期暴露期间，可能会改变 表示，因此，线性相关性的斜率。 使用中国 培养物中的仓鼠细胞和对6-硫鸟嘌呤的终点抗性， X射线和伽马射线在高剂量率和低剂量率下的突变将是 以确定修复过程在低剂量下是否明显 地区 长远来说，这项工作会扩大至包括其他 表型标记，人类细胞，和其他物理以及 化学诱导剂

For the population at large, the hazards due to biologically active agents in our environment--or associated with health services--are expected to result from low doses delivered over protracted periods. The hazards of main concern are those connected with cell inactivation, mutation, transformation, and altered differentiation. To estimate the degree of risk, it is customary to assume that the effect follows a linear or "single-hit" dose dependence whose rate may be inferred usually from an extrapolation to zero dose from effects produced by high doses delivered at high dose rates. Connected with the assumption of linearity is the implicit assumption that the magnitude of an effect is independent of the rate of dose delivery. This assumption comes from the conventional application of target theory, i.e., a single absorption event in the sensitive target produces the effect. As a consequence, sub-effective events are not registered and hence, biochemical/biological processes during or between exposures cannot modify the degree of effect. However, target theory as conventionally applied is only a limiting solution of a more general relationship according to which linearity also results if only a (dose-independent) fraction of the absorption events in the target is effective. Consequently bio-chemical/biological processes which occur during a protracted exposure may modify the proportion of events that are expressed and hence, the slope of the linear dependence. Using Chinese hamster cells in culture and the endpoint resistance to 6-thioguanine, mutations at high and at low dose rates by X- and Gamma-rays will be compared to determine if repair processes are evident in the low dose region. In the longer term, the work will be broadened to include other phenotypic markers, to human cells, and to other physical as well as to chemical inducers.