Tihan T, Elford H L, Cory J G
Department of Internal Medicine, University of South Florida College of Medicine, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612.
Adv Enzyme Regul. 1991;31:71-83. doi: 10.1016/0065-2571(91)90009-b.
Didox and Amidox inhibit L1210 cell growth in culture. At least one of the mechanisms in the mode(s) of action of the compounds is directed at the ribonucleotide reductase site. Partially purified preparations of ribonucleotide reductase activity are inhibited by Amidox and Didox. The formation of deoxycytidine nucleotides from [14C]cytidine in intact L1210 cells is also blocked. Didox and Amidox cause the decrease in the intracellular pools of the four dNTPs. Hydroxyurea-resistant L1210 cells are not cross-resistant to either Didox or Amidox. These data suggest that Didox and Amidox are not inhibiting ribonucleotide reductase through a mechanism similar to hydroxyurea.
双吖啶和氨吖啶在培养中抑制L1210细胞生长。这些化合物作用模式中的至少一种机制针对核糖核苷酸还原酶位点。氨吖啶和双吖啶可抑制核糖核苷酸还原酶活性的部分纯化制剂。完整L1210细胞中由[14C]胞苷形成脱氧胞苷核苷酸的过程也受到阻断。双吖啶和氨吖啶导致四种脱氧核苷三磷酸的细胞内池减少。羟基脲抗性L1210细胞对双吖啶或氨吖啶均无交叉抗性。这些数据表明,双吖啶和氨吖啶不是通过类似于羟基脲的机制抑制核糖核苷酸还原酶。