Scott D, Zampetti-Bosseler F
Int J Radiat Biol Relat Stud Phys Chem Med. 1980 Jan;37(1):33-47. doi: 10.1080/09553008014550041.
The ultrasensitivity of a subline of L5178Y mouse lymphoma cells to X-rays was thought to result from chromosome structural aberrations which are much more frequent in these cells than in radiation-resistant cells derived from them (Scott, Fox and Fox 1974). However, Ehmann, Nagasawa, Peterson and Lett (1974) in time-lapse photography studies of the sensitive line, concluded that the induction of multipolar mitoses by X-rays might be a more important mechanism of cell killing than chromosome aberrations. We have now shown that at survival levels above about 20 per cent, chromosome structural aberrations which lead to bridges and fragments at anaphase are about four times more frequent than spindle defects. We have confirmed the higher frequency of structural aberrations and spindle defects, and the greater mitotic delay in the X-ray-sensitive than in the X-ray-resistant cell line and have proposed a model which causally relates these end-points to cell killing and DNA repair.
L5178Y小鼠淋巴瘤细胞的一个亚系对X射线超敏感，被认为是由染色体结构畸变导致的，这些畸变在这些细胞中比在由它们衍生而来的抗辐射细胞中更为频繁（斯科特、福克斯和福克斯，1974年）。然而，埃曼、长泽、彼得森和莱特（1974年）在对敏感细胞系进行的延时摄影研究中得出结论，X射线诱导多极有丝分裂可能是比染色体畸变更重要的细胞杀伤机制。我们现在已经表明，在存活率高于约20%时，导致后期桥和片段的染色体结构畸变比纺锤体缺陷频繁约四倍。我们已经证实了X射线敏感细胞系中结构畸变和纺锤体缺陷的频率更高，以及有丝分裂延迟比X射线抗性细胞系更大，并提出了一个将这些终点与细胞杀伤和DNA修复因果相关的模型。
