3-氨基苯甲酰胺对紫外线诱导的DNA切除修复过程的影响。

Effect of 3-aminobenzamide on the process of ultraviolet-induced DNA excision repair.

作者信息

Otsuka F, Yamada K, Ohno H, Enomoto T, Hanaoka F, Ohsawa M, Yamada M

出版信息

Mutat Res. 1986 Jun;161(1):75-82. doi: 10.1016/0027-5107(86)90101-6.

Abstract

The effect of 3-aminobenzamide, a potent inhibitor of poly(ADP-ribosyl)ation, on UV-induced DNA excision repair was investigated. HeLa cells were treated with DNA replication inhibitors, hydroxyurea (HU) and 1-beta-D-arabinofuranosyl cytosine (araCyt), before and after ultraviolet light (UV) irradiation, to accumulate DNA single-strand breaks. The activity of poly(ADP-ribosyl)ation measured in the permeable cell system of HeLa cells was enhanced in a UV dose-dependent manner after the combined treatment with HU and araCyt in vivo. However, DNA repair synthesis in vitro was not affected by addition of 1 mM 3-aminobenzamide or nicotinamide, while incorporation of [3H]NAD in the same system was completely inhibited. Furthermore, neither the magnitude of UV-induced DNA single-strand breaks accumulated by the combined treatment of HU and araCyt nor the rate of their rejoining after release from the HU and araCyt block were influenced even in the presence of 10 mM 3-aminobenzamide. As the cytotoxicity of UV irradiation was significantly potentiated by 5 mM 3-aminobenzamide, these results suggest that poly(ADP-ribosyl)ation is involved in a process other than DNA excision repair induced by UV irradiation.

摘要

研究了聚（ADP - 核糖基）化的强效抑制剂3 - 氨基苯甲酰胺对紫外线诱导的DNA切除修复的影响。在紫外线（UV）照射之前和之后，用DNA复制抑制剂羟基脲（HU）和1 - β - D - 阿拉伯呋喃糖基胞嘧啶（araCyt）处理HeLa细胞，以积累DNA单链断裂。在体内用HU和araCyt联合处理后，在HeLa细胞的可渗透细胞系统中测得的聚（ADP - 核糖基）化活性以紫外线剂量依赖性方式增强。然而，体外DNA修复合成不受添加1 mM 3 - 氨基苯甲酰胺或烟酰胺的影响，而在同一系统中[3H]NAD的掺入被完全抑制。此外，即使存在10 mM 3 - 氨基苯甲酰胺，HU和araCyt联合处理积累的紫外线诱导的DNA单链断裂的程度及其从HU和araCyt阻断释放后的重新连接速率也不受影响。由于5 mM 3 - 氨基苯甲酰胺显著增强了紫外线照射的细胞毒性，这些结果表明聚（ADP - 核糖基）化参与了紫外线照射诱导的DNA切除修复以外的过程。