Effects of beta-arabinofuranosyladenine on the growth and repair of potentially lethal damage in Ehrilch ascites tumor cells.

Effects of beta-arabinofuranosyladenine on the growth and repair of potentially lethal damage in Ehrilch ascites tumor cells.
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β-阿拉伯呋喃糖腺嘌呤对埃里希腹水肿瘤细胞生长和潜在致命损伤修复的影响。

DOI:
10.2307/3575335
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发表时间:
1980
期刊:
影响因子:
3.4
通讯作者:
G. Iliakis
G. Iliakis
中科院分区:
医学3区
文献类型:
--
作者:
G. Iliakis

文献摘要

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β-D-Arabinofuranosyladenine (β-araA) 通过 DNA 聚合酶选择性抑制 DNA 合成来抑制艾利希腹水肿瘤细胞的生长。 RNA和蛋白质合成没有受到显着影响。照射后向细胞中添加 β-araA 会导致存活率呈浓度依赖性下降,这可能是由于抑制了潜在致命损伤的修复。由于 β-araA 选择性抑制 DNA 聚合酶,因此表明潜在致命损伤的修复涉及 DNA 水平上需要一些聚合的步骤。这些修复步骤在 DNA 中发生的速度与修复潜在致命损伤的速度相当。通过添加脱氧腺苷来改变 β-araA 对潜在致命损伤修复的抑制作用;这支持了 β-araA 在分子水平上与 dATP 竞争的发现。 β-araA 对潜在致命损伤修复的抑制作用是部分可逆的,导致集中...
β-D-Arabinofuranosyladenine (β-araA) inhibits the growth of Ehrlich ascites tumor cells by selective inhibition of DNA synthesis via DNA polymerases. RNA and protein synthesis are not significantly affected. Addition of β-araA to the cells after irradiation resulted in a concentration-dependent decrease in survival, presumably due to the inhibition of the repair of potentially lethal damage. Since β-araA selectively inhibits DNA polymerases it is suggested that repair of potentially lethal damage involves steps at the DNA level which require some polymerization. These repair steps take place in the DNA with a velocity comparable to that of the repair of potentially lethal damage. The inhibition of the repair of potentially lethal damage by β-araA was modified by the addition of deoxyadenosine; this supports the finding that β-araA acts competitively against dATP at the molecular level. The inhibition of the repair of potentially lethal damage by β-araA, which is partly reversible, resulted in a concentrat...