Palitti F, Tanzarella C, Degrassi F, De Salvia R, Fiore M, Natarajan A T
Mutat Res. 1983 Aug;110(2):343-50. doi: 10.1016/0027-5107(83)90151-3.
CHO cells were treated in G1 stage of the cell cycle with chromosome-breaking agents that act in an S-dependent manner. The cells were challenged in G2 stage, before fixation, with various inhibitors of DNA synthesis or repair. Short-wave UV, mitomycin C, decarbomyl mitomycin and 4-nitroquinoline oxide (4NQO) were used as chromosome-breaking agents. The inhibitors of DNA repair or synthesis used were hydroxyurea, aphidicolin and caffeine. Permeabilization of cells followed by a treatment with Neurospora endonuclease (a treatment to convert DNA single-strand breaks into double-strand breaks) did not have any influence on the frequencies of chromatid aberrations induced by the chemicals used, whereas with the inhibitors the extent of potentiation varied depending on the mutagen and the inhibitor used.
在细胞周期的G1期,用依赖于S期起作用的染色体断裂剂处理CHO细胞。在固定之前的G2期,用各种DNA合成或修复抑制剂对细胞进行处理。短波紫外线、丝裂霉素C、脱羰丝裂霉素和4-硝基喹啉氧化物(4NQO)用作染色体断裂剂。所使用的DNA修复或合成抑制剂为羟基脲、阿非迪霉素和咖啡因。细胞通透后用粗糙脉孢菌内切核酸酶处理(一种将DNA单链断裂转化为双链断裂的处理方法),对所用化学物质诱导的染色单体畸变频率没有任何影响,而对于抑制剂,增强程度则因诱变剂和所用抑制剂的不同而有所变化。