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1-亚硝基-8-硝基芘在大肠杆菌中的作用:在缺乏核苷酸切除修复的情况下DNA加合物的形成及突变后果

The action of 1-nitroso-8-nitropyrene in Escherichia coli: DNA adduct formation and mutational consequences in the absence of nucleotide excision-repair.

作者信息

Lambert I B, Gordon A J, Bryant D W, Glickman B W, McCalla D R

机构信息

Department of Biochemistry, McMaster University, Hamilton, Ontario, Canada.

出版信息

Carcinogenesis. 1991 May;12(5):879-84. doi: 10.1093/carcin/12.5.879.

DOI:10.1093/carcin/12.5.879
PMID:2029753
Abstract

To study the mechanisms of mutagenesis by the carcinogen 1,8-dinitropyrene we have determined the DNA adducts formed and mutations induced by its partially activated metabolite 1-nitroso-8-nitropyrene (1,8-NONP) in an Escherichia coli strain deficient in nucleotide excision-repair. Using DNA sequence analysis we have characterized a collection of 159 lacI- mutations recovered following treatment with 1,8-NONP. The mutational spectrum was dominated by -1 frameshifts (110 events) in runs of contiguous G or C residues. Frameshift frequency was observed to increase with the length of the reiterated sequence. Two mutations involved the loss of GpC from alternating (GpC)n sequences. The ratio of -1:-2 events observed following 1,8-NONP treatment was markedly different from that induced by N-acetoxy-N-acetyl-2-aminofluorene in the same genetic target. Other mutational classes recovered included 'spontaneous' hotspot mutations (19 events), base substitutions (12 events), deletions (7 events), one duplication, one + (A:T) frameshift and one mutation containing closely juxtaposed -(G:C) events. Of the 125 point mutations characterized, 124 occurred at G:C sites. The site specificity of mutation was consistent with the 32P-postlabeling profile of 1,8-NONP-DNA adducts which showed that 95% of the adducts migrated to the same position on the TLC plates as the guanine C(8) adduct 1-N-(2'-deoxyguanosin-8-yl)-amino-8-nitropyrene. Two minor 1,8-NONP-DNA mutations were also detected, one at dG/dC sites, and the other at dA/dT sites.

摘要

为了研究致癌物1,8 - 二硝基芘的诱变机制,我们测定了其部分活化代谢物1 - 亚硝基 - 8 - 硝基芘(1,8 - NONP)在缺乏核苷酸切除修复的大肠杆菌菌株中形成的DNA加合物和诱导的突变。通过DNA序列分析,我们对用1,8 - NONP处理后回收的159个lacI - 突变进行了特征描述。突变谱以连续G或C残基序列中的 - 1移码(110个事件)为主。观察到移码频率随重复序列长度的增加而增加。两个突变涉及交替(GpC)n序列中GpC的缺失。1,8 - NONP处理后观察到的 - 1: - 2事件的比率与在相同遗传靶点中由N - 乙酰氧基 - N - 乙酰 - 2 - 氨基芴诱导的比率明显不同。回收的其他突变类型包括“自发”热点突变(19个事件)、碱基取代(12个事件)、缺失(7个事件)、一个重复、一个 + (A:T)移码和一个包含紧密相邻的 - (G:C)事件的突变。在表征的125个点突变中,124个发生在G:C位点。突变的位点特异性与1,8 - NONP - DNA加合物的32P后标记图谱一致,该图谱表明95%的加合物在TLC板上迁移到与鸟嘌呤C(8)加合物1 - N - (2'-脱氧鸟苷 - 8 - 基) - 氨基 - 8 - 硝基芘相同的位置。还检测到两个次要的1,8 - NONP - DNA突变,一个在dG/dC位点,另一个在dA/dT位点。

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引用本文的文献

1
Carcinogen-induced frameshift mutagenesis in repetitive sequences.致癌物诱导的重复序列中的移码突变
Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1310-4. doi: 10.1073/pnas.89.4.1310.
2
A umuDC-independent SOS pathway for frameshift mutagenesis.一种不依赖umuDC的移码诱变SOS途径。
Mol Gen Genet. 1992 Nov;235(2-3):373-80. doi: 10.1007/BF00279383.
3
The influence of local DNA sequence and DNA repair background on the mutational specificity of 1-nitroso-8-nitropyrene in Escherichia coli: inferences for mutagenic mechanisms.
局部DNA序列和DNA修复背景对大肠杆菌中1-亚硝基-8-硝基芘突变特异性的影响:诱变机制推断
Genetics. 1992 Dec;132(4):911-27. doi: 10.1093/genetics/132.4.911.