Iqbal Z M, Majdan M, Epstein S S
Cancer Res. 1976 Mar;36(3):1108-13.
In vitro exposure of guinea pig pancreatic slices to 4-hydroxyaminoquinoline 1-oxide (HAQO) resulted in increased [methyl-3H]thymidine ([3H]TdR) incorporation into DNA, both in the presence and absence of hydroxyurea (HU). Normal DNA replicative synthesis, but not DNA repair synthesis, was suppressed by HU. The increase in [3H]TdR incorporation into DNA damage induced by HAQO. Exposure of pancreatic slices to 10(-6) to 10(-5) M concentrations of HAQO did not significantly increase thymidine incorporation; however, a 15-min exposure to 10(-4) M HAQO induced a significant increase in HU-insensitive [3H]TdR incorporation into DNA. Kinetics of [3H]TdR incorporation suggests that most of the DNA repair synthesis occurs during the 2 hr following HAQO-induced DNA damage.
将豚鼠胰腺切片在体外暴露于4-羟基氨基喹啉1-氧化物(HAQO),无论有无羟基脲(HU)存在,均导致[甲基-3H]胸苷([3H]TdR)掺入DNA增加。正常的DNA复制性合成而非DNA修复合成被HU抑制。[3H]TdR掺入DNA的增加是由HAQO诱导的DNA损伤所致。将胰腺切片暴露于10^(-6)至10^(-5) M浓度的HAQO不会显著增加胸苷掺入;然而,15分钟暴露于10^(-4) M HAQO会诱导HU不敏感的[3H]TdR掺入DNA显著增加。[3H]TdR掺入的动力学表明,大多数DNA修复合成发生在HAQO诱导的DNA损伤后的2小时内。