Farzaneh F, Feon S, Lebby R A, Brill D, David J C, Shall S
Nucleic Acids Res. 1987 Apr 24;15(8):3503-13. doi: 10.1093/nar/15.8.3503.
The human promyelocytic cell line, HL-60, shows large changes in endogenous poly(ADP-ribose) and in nuclear ADP-ribosyl transferase activity (ADPRT) during its induced myelocytic differentiation. DNA strand-breaks are an essential activator for this enzyme; and transient DNA strand breaks occur during the myelocytic differentiation of HL-60 cells. We have tested the hypothesis that these post-mitotic, terminally differentiating cells are less efficient in DNA repair, and specifically in DNA strand rejoining, than their proliferating precursor cells. We have found that this hypothesis is not tenable. We observe that there is no detectable reduction in the efficiency of DNA excision repair after exposure to either dimethyl sulphate or gamma-irradiation in HL-60 cells induced to differentiate by dimethyl sulphoxide. Moreover, the efficient excision repair of either dimethyl sulphate or gamma-irradiation induced lesions, both in the differentiated and undifferentiated HL-60 cells, is blocked by the inhibition of ADPRT activity.
人早幼粒细胞系HL-60在其诱导的髓细胞分化过程中，内源性聚（ADP-核糖）和核ADP-核糖基转移酶活性（ADPRT）显示出巨大变化。DNA链断裂是该酶的重要激活剂；并且在HL-60细胞的髓细胞分化过程中会发生短暂的DNA链断裂。我们检验了这样一个假设，即这些有丝分裂后终末分化的细胞在DNA修复方面，特别是在DNA链重新连接方面，比其增殖的前体细胞效率更低。我们发现这个假设是站不住脚的。我们观察到，用二甲基亚砜诱导分化的HL-60细胞在暴露于硫酸二甲酯或γ射线后，DNA切除修复效率没有可检测到的降低。此外，在分化和未分化的HL-60细胞中，硫酸二甲酯或γ射线诱导损伤的有效切除修复都被ADPRT活性的抑制所阻断。
