Porfirio B, Dallapiccola B, Gandini E
Mutat Res. 1985 Dec;144(4):257-63. doi: 10.1016/0165-7992(85)90061-2.
The cytogenetic effect of the DNA polymerase alpha inhibitor aphidicolin (APC) at a dose which did not affect cell cycle progression was determined in normal and Fanconi's anemia (FA) lymphocytes. APC enhanced sister-chromatid exchange (SCE) levels by about twice both in control and FA cells, while the yields of chromosome breakage increased up to 20 times in normal lymphocytes and 4 times in FA cells. APC did not act synergistically with the bifunctional alkylating diepoxybutane in terms of SCE either in normal or in FA lymphocytes. However, chromosome aberrations in cultures from normal subjects were much more than expected by an additive mode of action.
在正常淋巴细胞和范可尼贫血（FA）淋巴细胞中，测定了DNA聚合酶α抑制剂阿非迪霉素（APC）在不影响细胞周期进程剂量下的细胞遗传学效应。在对照细胞和FA细胞中，APC均使姐妹染色单体交换（SCE）水平提高了约两倍，而染色体断裂率在正常淋巴细胞中增加了20倍，在FA细胞中增加了4倍。在正常或FA淋巴细胞中，就SCE而言，APC与双功能烷化剂二环氧丁烷不存在协同作用。然而，正常受试者培养物中的染色体畸变比相加作用模式预期的要多得多。
