Bhattacharjee S B, Bhattacharyya N
Carcinogenesis. 1986 Aug;7(8):1267-71. doi: 10.1093/carcin/7.8.1267.
The effect of nicotinamide or benzamide, inhibitors of poly(ADP-ribose)polymerase activity, on X-ray and ultraviolet light induced killing of asynchronously dividing V79 Chinese hamster cells was to reduce the shoulder width of the survival curve; the rate of killing remaining unchanged and the yield of 8-azaguanine resistant mutants also remaining unaffected. However, when density inhibited cells were irradiated with X-rays or u.v. light, holding at this density allowed potentially lethal damage recovery (PLDR) to occur, enhancing survival. Inhibitors of poly(ADP-ribose)polymerase suppressed PLDR and also increased the yield of mutants. Thus the role of poly(ADP-ribose) in X-ray or u.v. induced killing and mutation was dependent on the condition of growth.
聚(ADP - 核糖)聚合酶活性抑制剂烟酰胺或苯甲酰胺对X射线和紫外线诱导的异步分裂的V79中国仓鼠细胞杀伤作用的影响是减小存活曲线的肩宽;杀伤速率保持不变,且对8 - 氮杂鸟嘌呤抗性突变体的产量也无影响。然而,当对密度抑制的细胞进行X射线或紫外线照射时,维持该密度可使潜在致死性损伤修复(PLDR)发生,从而提高存活率。聚(ADP - 核糖)聚合酶抑制剂可抑制PLDR并增加突变体的产量。因此,聚(ADP - 核糖)在X射线或紫外线诱导的杀伤和突变中的作用取决于生长条件。