Iliakis G, Wright E, Roberts W K, Ngo F Q
Radiat Res. 1986 Oct;108(1):23-33.
Expotentially growing and plateau-phase V79 cells were exposed to various doses of neutrons and plated either immediately or after treatment in hypertonic medium (250-500 mM NaCl) to express radiation-induced potentially lethal damage (PLD). Postirradiation treatment of exponentially growing cells in hypertonic medium (500 mM) resulted in a decrease in both Dq and D0, whereas postirradiation treatment of plateau-phase cells in hypertonic medium (in the range between 200 to 1,500 mM) resulted mainly in a reduction of Dq. This difference in response between exponentially growing and plateau-phase cells may reflect differences in the chromatin structure in cells at various stages of the cell cycle, affecting fixation of radiation-induced damage. Exposure of plateau-phase cells to gamma rays, on the other hand, resulted in a treatment time and salt concentration-dependent decrease in Dq along with a decrease in D0. Repair of neutron-induced, hypertonic treatment-sensitive PLD, measured by delaying treatment for various periods after irradiation, was found to proceed with a t1/2 of about 1 h. This is similar to the repair kinetics obtained by delaying treatment of plateau-phase cells with 150 microM beta-D-arabinofuranosyladenine (araA) after exposure to gamma rays or neutrons and contrasts the repair kinetics observed after exposure of cells to gamma rays. In this case, hypertonic treatment was found to affect a form of PLD repaired with a t1/2 of 10-15 min (beta-PLD) and araA, a different form of PLD, repaired with a t1/2 of about 1 h (alpha-PLD). Based on these results it is hypothesized that the sector of lesions affected by hypertonic treatment and araA coincides after exposure to neutrons (effect on alpha-PLD) but only partly overlaps after exposure to gamma rays (due to the effect on beta-PLD of hypertonic treatment). The results presented, together with previously published observations, suggest a differential induction and/or fixation by hypertonic medium of the alpha- and beta-PLD forms as the LET of the radiation increases. Furthermore, they indicate that direct comparison of the effects of a postirradiation treatment, as well as of the repair kinetics obtained by its delayed application after exposure to radiations of various LET, should be made with caution.
将指数生长期和平稳期的V79细胞暴露于不同剂量的中子下，然后立即接种，或在高渗培养基（250 - 500 mM NaCl）中处理后接种，以表达辐射诱导的潜在致死性损伤（PLD）。在高渗培养基（500 mM）中对指数生长期细胞进行辐照后处理，导致Dq和D0均降低，而在高渗培养基（200至1500 mM范围内）中对平稳期细胞进行辐照后处理，主要导致Dq降低。指数生长期和平稳期细胞在反应上的这种差异可能反映了细胞周期不同阶段细胞染色质结构的差异，影响辐射诱导损伤的固定。另一方面，将平稳期细胞暴露于γ射线，导致Dq随处理时间和盐浓度的增加而降低，同时D0也降低。通过在辐照后不同时间段延迟处理来测量中子诱导的、对高渗处理敏感的PLD的修复，发现其以约1小时的t1/2进行。这与在暴露于γ射线或中子后用150 microM β-D-阿拉伯呋喃糖基腺嘌呤（araA）延迟处理平稳期细胞所获得的修复动力学相似，并且与细胞暴露于γ射线后观察到的修复动力学形成对比。在这种情况下，发现高渗处理会影响一种以10 - 15分钟的t1/2进行修复的PLD形式（β-PLD），而araA会影响另一种以约1小时的t1/2进行修复的PLD形式（α-PLD）。基于这些结果，推测在暴露于中子后（对α-PLD的影响），高渗处理和araA影响的损伤区域重合，但在暴露于γ射线后（由于高渗处理对β-PLD的影响）仅部分重叠。所呈现的结果与先前发表的观察结果一起表明，随着辐射线性能量传递（LET）的增加，高渗培养基对α-和β-PLD形式的诱导和/或固定存在差异。此外，它们表明，对于辐照后处理的效果以及在暴露于不同LET的辐射后通过延迟应用所获得的修复动力学进行直接比较时应谨慎。
