Amundson S A, Chen D J
National Cancer Institute, National Institudes of Health, Bethesda, MD 20892, USA.
Int J Radiat Biol. 1996 May;69(5):555-63. doi: 10.1080/095530096145562.
In order to define further the effects of differences in recombinational proficiency on cell survival and mutation by ionizing radiation, we exposed the syngenic cell lines TK6 and WTK1 to continuous low dose-rate gamma-irradiation. We previously demonstrated that acute X-ray exposure results in lower survival and lower mutation induction at both the thymidine kinase (tk) and the hypoxanthine-guanine phosphoribosyltransferase (hprt) loci in TK6 cells compared with WTK1 cells. These differences were attributed in part to reduced levels of recombination in the TK6 line relative to WTK1. Using a low dose rate 137Cs irradiator, we exposed asynchronous growing populations of these cells to gamma-rays at 14.3, 6.7 and 2.7 cGy/h. Both cell lines exhibited a dose-rate effect on survival. Compared with acute doses, the low dose-rates also protected against mutation induction at the hrpt locus in WTK1, but protection was inversely related to dose-rate. There was also a slight inverse dose-rate effect in TK6, with mutation induction at the lowest dose-rate exceeding that at acute exposures.
为了进一步明确重组能力差异对电离辐射所致细胞存活及突变的影响，我们将同基因细胞系TK6和WTK1暴露于连续低剂量率的γ射线照射下。我们之前证明，与WTK1细胞相比，急性X射线照射导致TK6细胞在胸苷激酶（tk）和次黄嘌呤-鸟嘌呤磷酸核糖转移酶（hprt）位点的存活率更低，且突变诱导率更低。这些差异部分归因于TK6细胞系相对于WTK1细胞系的重组水平降低。使用低剂量率的137Cs辐照仪，我们将这些细胞的非同步生长群体暴露于14.3、6.7和2.7 cGy/h的γ射线下。两个细胞系均表现出剂量率对存活的影响。与急性剂量相比，低剂量率还能防止WTK1细胞在hprt位点发生突变诱导，但这种保护作用与剂量率呈负相关。TK6细胞也有轻微的剂量率负效应，最低剂量率下的突变诱导率超过急性照射时的突变诱导率。
