Frankenberg D, Kühn H, Frankenberg-Schwager M, Lenhard W, Beckonert S
Klinische Strahlenbiologie und Strahlenphysik, University of Göttingen, Germany.
Int J Radiat Biol. 1995 Dec;68(6):593-601. doi: 10.1080/09553009514551591.
Oncogenic transformation and inactivation were investigated in C3H10T1/2 mouse embryo fibroblasts exposed to proton-induced 0.28 keV carbon K (CK)-characteristic X-rays and 60Co gamma-rays as reference radiation at high dose-rate (2-3 and 0.7 Gy/min respectively). Both oncogenic cell transformation and cell inactivation followed a linear-quadratic relationship with dose. At low doses where the linear component dominates CK ultrasoft X-rays were more effective, by a factor of 4, at inducing oncogenic cell transformation and cell inactivation compared with 60Co gamma-rays. For both endpoints the RBE of CK ultrasoft X-rays gradually decreased with increasing dose mainly due to the greater quadratic component for 60Co gamma-rays compared with CK ultrasoft X-rays. Our experimental data are in agreement with the hypothesis that single DNA double-strand breaks (dsbs), which are induced by 0.28-keV ultrasoft CK X-rays, may lead to oncogenic cell transformation. With increasing absorbed dose, i.e. with decreasing mean distance between dsbs induced by 0.28-keV ultrasoft X-rays, oncogenic cell transformation and cell inactivation may also be induced by interaction between those dsbs.
在暴露于质子诱导的0.28 keV碳K(CK)特征X射线和作为高剂量率(分别为2 - 3和0.7 Gy/min)参考辐射的60Coγ射线的C3H10T1/2小鼠胚胎成纤维细胞中研究了致癌转化和失活情况。致癌细胞转化和细胞失活均与剂量呈线性二次关系。在低剂量时,线性成分占主导,与60Coγ射线相比,CK超软X射线在诱导致癌细胞转化和细胞失活方面的效率高4倍。对于这两个终点,CK超软X射线的相对生物效应(RBE)随着剂量增加而逐渐降低,这主要是因为与CK超软X射线相比,60Coγ射线的二次成分更大。我们的实验数据与以下假设一致:由0.28 keV超软CK X射线诱导的单个DNA双链断裂(dsb)可能导致致癌细胞转化。随着吸收剂量增加,即随着由