Chen Y, Goz B
Department of Pharmacology, University of North Carolina, School of Medicine, Chapel Hill 27514.
Anticancer Res. 1991 Jan-Feb;11(1):301-4.
1-beta-D-Arabinofuranosylcytosine (araC) caused concentration- and time--dependent single-strand breaks in SV28 cell DNA. Over the same concentration and time range, araC enhances the frequency of resistance to N-phosphonoacetyl-L-aspartate (PALA) and is also cytocidal (1). Comparison of induction of single-strand breaks by araC with its ability either to enhance the frequency of PALA-resistance or to kill cells, however, showed no obvious correlation, whether at different araC concentrations or exposure times. We conclude from these data that if there is a correlation between the ability of araC to cause single-strand breaks and either enhance PALA-resistance frequency or kill cells it is a complicated one or is masked by other events.
1-β-D-阿拉伯呋喃糖基胞嘧啶(阿糖胞苷,araC)可导致SV28细胞DNA出现浓度和时间依赖性的单链断裂。在相同的浓度和时间范围内,阿糖胞苷可提高对N-膦酰乙酰-L-天冬氨酸(PALA)的耐药频率,并且具有细胞毒性(1)。然而,比较阿糖胞苷诱导单链断裂的能力与其提高PALA耐药频率或杀伤细胞的能力,无论是在不同的阿糖胞苷浓度还是暴露时间下,均未显示出明显的相关性。从这些数据我们得出结论,如果阿糖胞苷导致单链断裂的能力与提高PALA耐药频率或杀伤细胞的能力之间存在相关性,那么这种相关性是复杂的,或者被其他事件所掩盖。