Kirillova T V, Rozanov Iu M, Spivak I M
Tsitologiia. 1992;34(3):76-81.
A specific inhibitor of poly(ADP-ribose)polymerase-3-aminobenzamide (6 mM) has been shown to: 1) reduce survival of non-irradiated CHO-K1 cells, cultivated in medium containing 5-bromodeoxyuridine (10 mkM, BDU cells), and increase their radiosensitivity; 2) induce G2 delay in BDU cells while progressing through the cell cycle as analysed by the DNA flow cytometry; 3) increase to a great degree G2 delay in X-irradiated BDU cells. 3-Aminobenzamide is primarily effective when it is present during the first or two first cell cycles after the initial addition of BDU. The above data confirm the involvement, presumably an indirect one, of ADP-ribosylation in the DNA repair through affecting the chromatin structure.
聚(ADP - 核糖)聚合酶的特异性抑制剂——3 - 氨基苯甲酰胺(6 mM)已被证明:1)降低在含有5 - 溴脱氧尿苷(10 μM,BDU细胞)的培养基中培养的未辐照CHO - K1细胞的存活率,并增加其放射敏感性;2)通过DNA流式细胞术分析,在BDU细胞进入细胞周期时诱导G2期延迟;3)在X射线辐照的BDU细胞中极大地增加G2期延迟。3 - 氨基苯甲酰胺在最初添加BDU后的第一个或前两个细胞周期中存在时主要有效。上述数据证实了ADP - 核糖基化可能通过影响染色质结构间接参与DNA修复。