Department of Radiation Oncology, University of California-Irvine, CA 92697, USA.
Dose Response. 2006 Nov 27;4(4):302-8. doi: 10.2203/dose-response.06-114.Redpath.
A major concern of exposure to low doses of radiation is the risk of cancer induction. Epidemiologic data are rarely powerful enough to accurately discriminate this risk at doses <10 cGy. In order to gain insight into events at these low doses, laboratory-based studies of relevant endpoints are required. One such endpoint is radiation-induced neoplastic transformation in vitro. Such studies can provide quantitative dose-response data, as well as insights into underlying cellular and molecular mechanisms. Data are presented that indicate that low doses of low LET radiation can suppress neoplastic transformation in vitro to levels below those seen spontaneously. Mechanisms involved include both the death of a subpopulation of cells prone to spontaneous neoplastic transformation and the induction of DNA repair. The relative contributions of these mechanisms is dose-dependent. The relevance of these observations to radiation risk estimation is discussed.
人们主要关注的是低剂量辐射暴露的致癌风险。由于流行病学数据通常不够强大，无法在<10cGy 的剂量下准确区分这种风险。为了深入了解低剂量下的情况，需要进行基于实验室的相关终点研究。其中一个终点是体外辐射诱导的肿瘤转化。此类研究可以提供定量剂量-反应数据，并深入了解潜在的细胞和分子机制。有数据表明，低剂量低 LET 辐射可以抑制体外肿瘤转化，使其水平低于自发转化水平。所涉及的机制包括容易自发发生肿瘤转化的细胞亚群的死亡和 DNA 修复的诱导。这些机制的相对贡献取决于剂量。讨论了这些观察结果对辐射风险估计的相关性。
