Kufe D W, Major P P, Munroe D, Egan M, Herrick D
Cancer Res. 1983 May;43(5):2000-4.
We have used cesium sulfate density gradient centrifugation to monitor the incorporation of 9-beta-D-arabinofuranosyladenine (ara-A) into L1210 cellular nucleic acids. The results demonstrate the specific incorporation of ara-A in L1210 DNA. We have also found a highly significant relationship between the formation of ara-A incorporated into DNA and loss of clonogenic survival. This relationship was maintained when using ara-A in the presence of the adenosine deaminase inhibitor deoxycoformycin. Furthermore, treatment with increasing concentrations of ara-A resulted in a greater proportion of ara-A residues at the 3'-terminus, consistent with this agent providing a poor primer terminus for elongating DNA strands. These findings are similar to those obtained previously with 1-beta-D-arabinofuranosylcytosine and suggest that the incorporation of arabinofuranosyl derivatives in DNA is one mechanism responsible for cell lethality.
我们使用硫酸铯密度梯度离心法来监测9-β-D-阿拉伯呋喃糖基腺嘌呤（ara-A）掺入L1210细胞核酸的情况。结果表明ara-A可特异性掺入L1210 DNA中。我们还发现，ara-A掺入DNA的形成与克隆形成存活率的丧失之间存在高度显著的关系。当在腺苷脱氨酶抑制剂脱氧助间型霉素存在的情况下使用ara-A时，这种关系得以维持。此外，用浓度不断增加的ara-A进行处理导致3'-末端的ara-A残基比例更高，这与该药物为延长DNA链提供不良引物末端一致。这些发现与先前用1-β-D-阿拉伯呋喃糖基胞嘧啶获得的结果相似，并表明阿拉伯呋喃糖基衍生物掺入DNA是导致细胞致死的一种机制。
