Wang C Y, Linsmaier-Bednar E M, Garner C D
Chem Biol Interact. 1982 Oct;42(1):79-84. doi: 10.1016/0009-2797(82)90143-0.
Primary cultures of rat urothelial cells were exposed to hydroxyurea, [3H]thymidine, and 4-nitroquinoline 1-oxide (NQO) or N-hydroxy-4-aminoquinoline 1-oxide (HAQO) in a serum-free media for 2 h; unscheduled DNA synthesis (UDS) was measured by autoradiography. Both NQO and HAQO produced unscheduled DNA synthesis. Dicumarol, an inhibitor of NQO nitroreductase, inhibited the activity of NQO and, to a lesser extent, HAQO. Pyrophosphate, an inhibitor of seryl-AMP synthetase, inhibited the activity of both compounds. Neither dicumarol nor pyrophosphate, under similar experimental conditions, inhibited the activity of N-hydroxy-N-2-acetylaminofluorene (N-OH-AAF). These results support the idea that nitro-reductase and seryl-AMP synthetase may be involved in the activation of NQO.
将大鼠膀胱上皮细胞的原代培养物在无血清培养基中暴露于羟基脲、[3H]胸腺嘧啶核苷、4-硝基喹啉 1-氧化物（NQO）或 N-羟基-4-氨基喹啉 1-氧化物（HAQO）2 小时；通过放射自显影法测量非预定 DNA 合成（UDS）。NQO 和 HAQO 均产生了非预定 DNA 合成。双香豆素是 NQO 硝基还原酶的抑制剂，它抑制了 NQO 的活性，对 HAQO 的抑制作用较小。焦磷酸是丝氨酰-AMP 合成酶的抑制剂，它抑制了这两种化合物的活性。在相似的实验条件下，双香豆素和焦磷酸均未抑制 N-羟基-N-2-乙酰氨基芴（N-OH-AAF）的活性。这些结果支持了硝基还原酶和丝氨酰-AMP 合成酶可能参与 NQO 活化的观点。
