Kubota M, Tanizawa A, Hashimoto H, Shimizu T, Takimoto T, Kitoh T, Akiyama Y, Mikawa H
Department of Pediatrics, Kyoto University, Japan.
Leuk Res. 1990;14(4):371-5. doi: 10.1016/0145-2126(90)90165-6.
Treatment of human non-lymphoid cell lines, HL-60 and U937, with etoposide stimulated poly (ADP-ribose) synthesis three- to fourfold, whereas no significant effects were observed in the lymphoid cell lines, Molt4 and CEM. This was confirmed by either an increased uptake of radio-labelled NAD into the acid-insoluble fraction or a fall in cellular NAD levels, which was counteracted by 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase. On the other hand, another DNA damaging agent, N-methyl-N'-nitro-N-nitrosoguanidine augmented poly(ADP-ribose) synthesis equally in both cell types. These results taken together indicate that the activation of poly(ADP-ribose) synthesis following exposure to etoposide is a cell type specific phenomenon.
用依托泊苷处理人非淋巴细胞系HL - 60和U937，可使聚（ADP - 核糖）合成增加三到四倍，而在淋巴细胞系Molt4和CEM中未观察到显著影响。这通过放射性标记的NAD摄取到酸不溶性部分增加或细胞内NAD水平下降得到证实，而聚（ADP - 核糖）聚合酶抑制剂3 - 氨基苯甲酰胺可抵消这种下降。另一方面，另一种DNA损伤剂N - 甲基 - N'- 硝基 - N - 亚硝基胍在两种细胞类型中均能同等程度地增强聚（ADP - 核糖）合成。综合这些结果表明，暴露于依托泊苷后聚（ADP - 核糖）合成的激活是一种细胞类型特异性现象。
