Yamada H, Miyahara T, Sasaki Y F
Biological Laboratory, School of Science, Kwansei Gakuin University, Hyogo, Japan.
Mutat Res. 1993 Jul;302(3):137-45. doi: 10.1016/0165-7992(93)90039-x.
The co-clastogenic effect of cadmium ion (Cd2+) was studied in Chinese hamster CHO K1 cells and excision repair-deficient human XP20SSV cells. Cd2+ at < or = 28.0 microM did not show any clastogenic effects under the experimental conditions used. Cd2+ post-treatment at < or = 3.50 microM, however, increased the number of both breakage- and exchange-type chromatid aberrations induced by mitomycin C (MMC) and 4-nitroquinoline 1-oxide (4NQO) in CHO K1 cells. Enhancement of chromosome aberrations induced by MMC was observed when CHO K1 cells were treated with Cd2+ during the G1 phase. Cd2+ was also co-clastogenic with MMC in XP20SSV cells. Its co-clastogenic effect, however, was not observed in 4NQO-treated XP20SSV cells. These results suggest that Cd2+ inhibits DNA pre-replicational repair, perhaps DNA excision repair, thereby causing co-clastogenic effects.
在中国仓鼠CHO K1细胞和切除修复缺陷的人XP20SSV细胞中研究了镉离子（Cd2+）的共致断裂效应。在所用实验条件下，≤28.0微摩尔的Cd2+未显示出任何致断裂效应。然而，≤3.50微摩尔的Cd2+后处理增加了丝裂霉素C（MMC）和4-硝基喹啉1-氧化物（4NQO）在CHO K1细胞中诱导的断裂型和交换型染色单体畸变的数量。当CHO K1细胞在G1期用Cd2+处理时，观察到MMC诱导的染色体畸变增强。Cd2+在XP20SSV细胞中也与MMC有共致断裂作用。然而，在4NQO处理的XP20SSV细胞中未观察到其共致断裂效应。这些结果表明，Cd2+抑制DNA复制前修复，可能是DNA切除修复，从而导致共致断裂效应。
