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紫外线照射的腺病毒2的增强再激活与致癌物预处理的HeLa细胞中的诱变增强无关。

Enhanced reactivation of UV-irradiated adenovirus 2 is not associated with enhanced mutagenesis in carcinogen-pretreated HeLa cells.

作者信息

Piperakis S M

机构信息

Department of Biology, Nuclear Research Center Democritos, Agia Paraskevi, Athens, Greece.

出版信息

Mutat Res. 1987 Nov;192(3):203-6. doi: 10.1016/0165-7992(87)90056-x.

DOI:10.1016/0165-7992(87)90056-x
PMID:3120002
Abstract

Treatment of HeLa cells with low doses of the carcinogens aflatoxin B1, methyl methanesulfonate (MMS) or ethyl methanesulfonate (EMS) increases the survival rate of UV-irradiated adenovirus 2 (ade2). This increase is maximal if the time interval between cell treatment and virus infection is delayed by 36 h. No enhanced mutagenesis was found measuring the reversion frequency of a temperature-sensitive mutant of ade2 grown in HeLa cells treated with the same carcinogens. The enhanced viral reactivation observed does not, therefore, display a significant error-prone component.

摘要

用低剂量致癌物黄曲霉毒素B1、甲基磺酸甲酯（MMS）或乙基磺酸甲酯（EMS）处理HeLa细胞，可提高紫外线照射的腺病毒2（ade2）的存活率。如果细胞处理和病毒感染之间的时间间隔延迟36小时，这种增加将达到最大值。在用相同致癌物处理的HeLa细胞中培养的ade2温度敏感突变体的回复频率测量中，未发现诱变增强。因此，观察到的增强的病毒复活并不显示出明显的易错成分。

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Enhanced reactivation of UV-irradiated adenovirus 2 is not associated with enhanced mutagenesis in carcinogen-pretreated HeLa cells.紫外线照射的腺病毒2的增强再激活与致癌物预处理的HeLa细胞中的诱变增强无关。
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