Hagan M P, Han A, Smith V N
Br J Cancer Suppl. 1984;6:73-7.
BrdUrd pulse labelling of synchronous Chinese hamster cell cultures was used to correlate repair of sublethal damage with removal of alkali-labile lesions. Both processes were modified in a quantitatively similar manner by cysteamine. In addition, the age responses for repair of sublethal damage and for cysteamine reduction of repair agreed. Through the use of thymidine as an S-phase-blocking agent it was further demonstrated that progression past the S-phase of the cell cycle was required for the loss of resistance to UVB light in BrdUrd-substituted cells. Similarly, a thymidine block administered before synthesis upon the BrdUrd-substituted template prevented the cell from acquiring the sensitivity to UVB light normally associated with synthesis on a lesioned template. The UVB-light-sensitive mutant V79-UC was shown to have reduced capacities both for the accumulation of sublethal injury and for the removal of alkali-labile lesions. These data support the notion that alkali-labile lesions are responsible for sublethal damage in BrdUrd pulse-labelled Chinese hamster cells.
采用5-溴脱氧尿苷脉冲标记同步化的中国仓鼠细胞培养物，以将亚致死损伤的修复与碱不稳定损伤的去除相关联。半胱胺以定量相似的方式改变了这两个过程。此外，亚致死损伤修复的年龄反应与半胱胺对修复的减少作用一致。通过使用胸苷作为S期阻断剂，进一步证明了BrdUrd取代细胞中对UVB光的抗性丧失需要细胞周期S期的进展。同样，在BrdUrd取代模板上合成之前给予胸苷阻断可防止细胞获得通常与损伤模板上合成相关的对UVB光的敏感性。UVB光敏感突变体V79-UC显示出亚致死损伤积累和碱不稳定损伤去除的能力均降低。这些数据支持了碱不稳定损伤是BrdUrd脉冲标记的中国仓鼠细胞中亚致死损伤原因的观点。
