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[抑制4-硝基喹啉-1-氧化物诱导的慢性病毒感染人类细胞DNA断裂修复过程]

[Inhibition of the process of 4-nitroquinoline-1-oxide-induced DNA break repair in chronically virus-infected human cells].

作者信息

Zasukhina G D, Bogomolova N N, Vostrova N G, Kolonina I V, Desiatskova R G

出版信息

Vopr Virusol. 1981 Jan-Feb(1):94-7.

PMID:6789556
Abstract

Inhibition of DNA resynthesis after treatment of cell culture with 4-nitroquinoline-1-oxide was found to be due not to the induction of virus mutants repressing this system but to the selection in the cell population of cells predominantly with partially or completely defective system of reparation, or to the development of cellular reparative system because of the presence of viruses in the cell. In chronic infection of HEp-2 cells with tick-borne encephalitis, rubella, and rabies viruses the same phenomenon was observed, namely, inhibition of different stages of the reparation process, i.e. the mechanism of reparation is universal.

摘要

在用4-硝基喹啉-1-氧化物处理细胞培养物后,发现DNA再合成受到抑制,这并非是由于诱导了抑制该系统的病毒突变体,而是由于在细胞群体中选择了主要具有部分或完全缺陷修复系统的细胞,或者是由于细胞中存在病毒而导致细胞修复系统的发展。在用蜱传脑炎病毒、风疹病毒和狂犬病病毒对HEp-2细胞进行慢性感染时,也观察到了同样的现象,即修复过程不同阶段的抑制,也就是说,修复机制是普遍存在的。

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