Lunec J
Br J Cancer Suppl. 1984;6:13-8.
There is substantial evidence that ADP-ribosylation is stimulated in response to DNA strand breaks produced directly by a damaging agent or during excision repair processes. The report of a reduced stimulation of ADPRT activity in irradiated ataxia telangiectasia cells has recently stimulated a wide interest in the role of ADP-ribosylation in cellular radiation response. The resulting studies, some of which are presented at this conference, demonstrate that cellular recovery from radiation damage can be significantly impaired if ADP-ribosylation is inhibited to a sufficiently low level. The implication is that the repair of DNA lesions is affected. This review summarizes the involvement of the enzyme ADPRT and the extent of ADP-ribosylation in the repair of DNA damage and of cellular recovery.
有大量证据表明,在由损伤剂直接产生的DNA链断裂后或在切除修复过程中,ADP核糖基化会被激活。最近,关于辐射诱发的共济失调毛细血管扩张症细胞中ADPRT活性刺激降低的报道,引发了人们对ADP核糖基化在细胞辐射反应中作用的广泛关注。由此产生的一些研究(其中一些在本次会议上进行了展示)表明,如果将ADP核糖基化抑制到足够低的水平,细胞从辐射损伤中的恢复可能会受到显著损害。这意味着DNA损伤的修复受到了影响。本综述总结了ADPRT酶的参与情况以及ADP核糖基化在DNA损伤修复和细胞恢复中的程度。