Snyder R D
Biochem Biophys Res Commun. 1984 Oct 30;124(2):457-61. doi: 10.1016/0006-291x(84)91575-4.
3-Aminobenzamide does not deplete cellular purine deoxynucleoside triphosphate pools as do the structurally-related ribonucleotide reductase inhibitors, the hydroxy- and amino-substituted benzohydroxamic acids. Thus, the previously reported ability of 3-aminobenzamide to inhibit de novo synthesis of DNA purines does not appear to be due to a direct effect on pools via inhibition of ribonucleotide reductase. The enhancement rather than inhibition by 3-aminobenzamide of DNA repair in the present studies, however, leaves open the possibility that pool modulation may play a role in cell systems where repair inhibitory effects are seen.
与结构相关的核糖核苷酸还原酶抑制剂（羟基和氨基取代的苯甲羟肟酸）不同，3-氨基苯甲酰胺不会耗尽细胞中的嘌呤脱氧核苷三磷酸库。因此，先前报道的3-氨基苯甲酰胺抑制DNA嘌呤从头合成的能力似乎并非由于通过抑制核糖核苷酸还原酶对库产生直接影响。然而，在本研究中3-氨基苯甲酰胺对DNA修复起到增强而非抑制作用，这使得库调节可能在出现修复抑制作用的细胞系统中发挥作用这一可能性仍然存在。
