拓扑异构酶II抑制剂ICRF-193对紫外线诱导的染色体畸变形成的影响。

Effects of an inhibitor of topoisomerase II, ICRF-193 on the formation of ultraviolet-induced chromosomal aberrations.

作者信息

Ikushima T, Shima Y, Ishii Y

机构信息

Biology Division, Kyoto University of Education, 1 Fukakusa-Fujinomori-cho, Fushimi-ku, Kyoto 612-0863, Japan.

出版信息

Mutat Res. 1998 Aug 3;404(1-2):35-8. doi: 10.1016/s0027-5107(98)00092-x.

DOI:10.1016/s0027-5107(98)00092-x

PMID:9729258

Abstract

Treatments of Chinese hamster V79 cells during one cell cycle with a new type of topoisomerase II inhibitor, ICRF-193, which does not accumulate cleavable topoisomerase-DNA complexes induced both chromosome- and chromatid-type aberrations with high frequencies. Furthermore, ICRF-193 synergistically enhanced the yield of UVB-induced chromatid-type aberrations, chromatid exchanges in particular. Treated with ICRF-193 for the last 3 h before harvest, cells showed frequent incidence of chromatid-type aberrations and synergistic enhancement of UVB-induced chromatid-type aberrations, chromatid exchanges in particular. These results suggest that spontaneous and UVB-induced lesions might be ultimately transformed into chromatid-type aberrations by topoisomerase II-dependent checkpoint process(es) in the G2 phase of the cell cycle.

摘要

用新型拓扑异构酶II抑制剂ICRF - 193在一个细胞周期内处理中国仓鼠V79细胞，该抑制剂不会积累可裂解的拓扑异构酶 - DNA复合物，却能高频诱导染色体型和染色单体型畸变。此外，ICRF - 193协同增强了UVB诱导的染色单体型畸变的发生率，尤其是染色单体交换。在收获前最后3小时用ICRF - 193处理细胞，细胞显示出染色单体型畸变的频繁发生以及UVB诱导的染色单体型畸变（尤其是染色单体交换）的协同增强。这些结果表明，自发损伤和UVB诱导的损伤可能最终通过细胞周期G2期拓扑异构酶II依赖的检查点过程转化为染色单体型畸变。