Mechanism of synergistic cell killing by hydroxyurea and cytosine arabinoside.
Mechanism of synergistic cell killing by hydroxyurea and cytosine arabinoside.
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羟基脲和阿糖胞苷协同杀伤细胞的机制。
DOI：
10.20772/cancersci1985.76.8_729
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
S. Yoshida
中科院分区：
文献类型：
--
作者：
M. Tanaka;K. Kimura;S. Yoshida
当在1-β-D-阿拉伯呋喃糖基胞嘧啶（ara-C）之前给予羟基脲（HU）时，发生对人淋巴细胞白血病细胞系CCRF-CEM的协同细胞杀伤。在最佳剂量HU（1 mM）下，ara-CTP浓度增加4倍，细胞内ara-C积累增加4倍，而dCTP浓度降低50%以上。在循环血液中的人急性髓性白血病细胞中也观察到HU治疗后阿糖胞苷的细胞内积累增加。因此，HU和ara-C的协同细胞杀伤作用可能是在该酶的天然底物dCTP浓度降低的情况下，ara-CTP水平升高对DNA聚合酶的抑制作用增强的结果。这种协同作用不是由于阿糖胞苷掺入DNA的增加，因为用HU处理细胞并没有增强阿糖胞苷掺入DNA，而是抑制了它。
Synergistic cell killing of human lymphoblastic leukemia cell line, CCRF-CEM, occurred when hydroxyurea (HU) was administered before 1-beta-D-arabinofuranosylcytosine (ara-C). At the optimal dose of HU (1mM), the ara-CTP concentration increased 4-fold and the intracellular accumulation of ara-C increased 4-fold, while the dCTP concentration decreased by more than 50%. Increased intracellular accumulation of ara-C after HU treatment was also observed in human acute myelogenous leukemic cells in circulating blood. Therefore, the synergistic cell kill of HU and ara-C may be the consequence of greater inhibition of DNA polymerase by the increased level of ara-CTP in the presence of the decreased concentration of the natural substrate of this enzyme, dCTP. This synergism was not due to an increased incorporation of ara-C into DNA since the treatment of cells with HU did not enhance the ara-C incorporation into DNA but rather suppressed it.
羟基脲对 L1210 和 HL-60 细胞的生化和细胞因子调节以及对 1-β-D-阿拉伯呋喃糖基胞嘧啶代谢和细胞毒性的影响。
影响因子：
11.2
作者：
Rauscher3rd,F;Cadman,E
通讯作者：
Cadman,E
N-（膦乙酰基）-L-天冬氨酸对人白血病和正常骨髓祖细胞中 1-β-D-阿拉伯呋喃糖基胞嘧啶代谢和细胞毒性的差异作用。
影响因子：
11.2
作者：
Grant,S;Rauscher3rd,F;Cadman,E
通讯作者：
Cadman,E