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真核细胞染色质中的腺苷二磷酸核糖基转移酶(ADPRT)是维持有效DNA切除修复所必需的。本研究证明在通透化了的FL细胞中ADPRT活性呈细胞周期依存性波动。它的活性峰值见于DNA合成峰值后的4～6小时;同步培养于G_1期的细胞在按触DNA-损伤剂,甲基硝基亚硝基胍(MNNG)、甲磺酸甲酯(MMS)及4-硝基喹啉氧化物(4NQO)后ADPRT活性明显升高。在细胞周期的不同阶段,MNNG/4NQO对ADPRT的刺激作用与细胞周期对它的影响呈叠加作用。但MMS对ADPRT活性的刺激作用却完全依存于基础酶活性。在基础酶活性最高时,MMS几乎不显示其ADPRT刺激作用。因而认为DNA-损伤剂引起的ADPRT刺激作用有不止一个机制存在。同步于G_1期的细胞最适合于显示DNA损伤后的ADPRT活性升高。上述细胞周期性影响可能同细胞周期中DNA修复的顺序性变化以及细胞对致癌物敏感性的周期性变化有关。
Adenosine diphosphate ribosyltransferase (ADPRT) in eukaryotic chromatin is necessary to maintain efficient DNA excision repair. This study demonstrates that ADPRT activity in circulating FL cells fluctuates in a cell cycle-dependent manner. Its peak activity was found in 4 to 6 hours after the DNA synthesis peak; cells cultured in G 1 phase were significantly different in the groups of DNA-damaging agents, MNNG, MMS, And 4-nitroquinoline oxide (4NQO) ADPRT activity was significantly increased. At different stages of the cell cycle, the effects of MNNG / 4NQO on ADPRT are additive to the effects of the cell cycle on it. However, MMS stimulation of ADPRT activity is completely dependent on the activity of the basic enzyme. At the highest basal enzyme activity, MMS showed little or no ADPRT stimulating effect. Thus, there is more than one mechanism for ADPRT stimulation induced by DNA-damaging agents. Cells synchronized to the G_1 phase are best suited to show increased ADPRT activity after DNA damage. The above-mentioned cell cycle effects may be related to the sequential changes of DNA repair in the cell cycle and the periodic changes of the cell sensitivity to carcinogens.