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致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别

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居学海, 张琪, 戴乾圜. 致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别[J]. 环境化学, 2001, 20(6): 537-543.
引用本文: 居学海, 张琪, 戴乾圜. 致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别[J]. 环境化学, 2001, 20(6): 537-543.
shu
Ju Xuehai, Zhang Qi, Dai Qianhuan1 . NOTABLE DIFFERENCE ON INDUCING DNA INTERSTRANDCROSS-LINK BETWEEN MUTAGENIC CARCINOGENS ANDNON-CARCINOGENS[J]. Environmental Chemistry, 2001, 20(6): 537-543.
Citation: Ju Xuehai, Zhang Qi, Dai Qianhuan1 . NOTABLE DIFFERENCE ON INDUCING DNA INTERSTRANDCROSS-LINK BETWEEN MUTAGENIC CARCINOGENS ANDNON-CARCINOGENS[J]. Environmental Chemistry, 2001, 20(6): 537-543.
shu

致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别

  • 基金项目:

    国家自然科学基金资助项目(批准号:20042001)

NOTABLE DIFFERENCE ON INDUCING DNA INTERSTRANDCROSS-LINK BETWEEN MUTAGENIC CARCINOGENS ANDNON-CARCINOGENS

  • 1.

    Center of Environmental Sciences, Peking University, Beijing, 10087l;

  • 2.

    Center for Chemistry and Bioengineering of Cancer, Beijing Polytechnic University, Beijing, l00022

  • Fund Project:

  • 摘要: 借碱洗脱法证明：具有致突变能力的致癌剂1,2-二溴乙烷和肼在经过代谢活化后,均剂量相关地引起L1210细胞中DNA的股间交联。相反,动物致癌试验表现阴性的致突变剂溴乙烷,以及通过各种致癌动物试验均显示阴性的传统常用致突变剂羟胺,在代谢活化以后的同样条件下均不能引起L1210细胞中DNA的股间交联。这证明了双区理论的致癌机理观点,即致癌剂必须是双官能烷化剂,其同时引起互补碱对的交联将引起癌变。相反,股内单一碱基的变异则可能引起致突变作用。并用APCI/SIM(大气压化学电离/选择离子质谱)证明：1,2-二溴乙烷与DNA碱基对的模型反应,与致突实验一致主要引起G-C对的交联和发生G-C→A-T突变。
    Abstract: By means of DNA filter elution method, it is evidenced that two carcinogens 1,2-dibro-moethane with mutagenic potential and hydrazine with weak mutagenicity, can both induce the DNA interstrand cross-link with quantity dependence in L1210 culture. However in a identical condition, two non-carcinogens with analogous structures, ethylbromide and hydroxylamine with mutagenicity and potent mutagenicity respectively, both can't induce the corresponding cross-link. These results are consistent with the mechanism of the carcinogenesis of Dai's di-region theory that the carcinogen must be a bifunctional alkylating agent, the monofunctional damage of the base with single strand can only induce the mutagenesis but not carcinogenesis.
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  • [1] 戴乾圜,化学致癌剂及其化学致癌机理的研究.中国科学,1979,10:964-977
    [2] Dai Qianhuan,Di-Region Theory,New Discovery on Mechanism of Carcinogenesis.Molecular Engineering,1998,8:61-89
    [3] 戴乾圜,双区理论致癌机理和致癌剂的非经验定量结构生理效应关系.北京:科学出版社,2000
    [4] Kohn K W,DNA Filter Elution:a Window on DNA Damage in Mammalian Cells.Bioassays,1996,18:505-513
    [5] Guo Baochun,Mass Spectrometry in DNA Analysis.Anal.Chem.,1999,71(12):333R-337R
    [6] Mclafferty F W,Fridriksson E K,Horn D M et al.,Biochemistry,Biomolecule Mass Spectrometry.Science,1999,284(5418):1289-1290
    [7] International Agency for Research on Cancer.IARC Monographs on the Carcinogenic Risks of Chemicals to Humans.Lyon,France,1977,Vol.15,p195
    [8] Zedeck M S,Hydrazine Derivatives,Azo and Azoxy Compounds,and Methylazoxymethanol and Cycasin.In Chemical Carcinogens,Vol.Ⅱ,Ed.Searle C E,Amer.Chem.Soc.,Washington D C,1984,p 915-944
    [9] (a)Sinden R R,DNA Structure and Function.San Diego:Academic Press,1994,pp 38-46(b)Singer B R,Grunberger D,Molecular Biology of Mutagens and Carcinogens.New York,:Plenum Press,1984,pp 50-53
    [10] Maxam A M,Gilbert W,Sequencing End-Labeled DNA with Base-Specific Chemical Cleavages.Methods Enzymol.,1980,65:499-560
    [11] Pei Shu,Zhu Xujing,Xiang Mang et al.,The Cross-Linking Ability between DNA Double Strands as a New Method for the Identification of Carcinogens.In Recent Advances of Chemistry and Molecular Biology in Cancer Research.Ed,Dai Qianhuan,Margaret-Ann,Armour and Zheng Qingying.Beijing/Heideberg:Science Press/Springer-Verlag,1993,111-119
    [12] 戴乾圜,张庆荣,王丽慧等,化学致癌作用是一种DNA股间交联的若干实验证明.科学通报,1999,44(24):2624-2628;英文版2000,45(23):2125-2129


    [13] Ali-Osman F,Quenching of DNA Cross-Link Procursors of Chloroethylnitrosoureas and Attenuation of DNA Interstrand Cross-Link by Glutathione.Cancer Res.,1989,49:5258-5261
    [14] Tong W P,Kirk M C,Ludlum D B,Formation of the Cross-Link 1-[N3-deoxycytidyl]2-[N1-deoxyguanosinyl]-ethane in DNA Treated with NN′-Bis(2-chloroethyl)-N-nitrosourea.Cancer Res.,1982,42:3102-3105

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  • 收稿日期:  2001-03-03
居学海, 张琪, 戴乾圜. 致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别[J]. 环境化学, 2001, 20(6): 537-543.
引用本文: 居学海, 张琪, 戴乾圜. 致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别[J]. 环境化学, 2001, 20(6): 537-543.
shu
Ju Xuehai, Zhang Qi, Dai Qianhuan1 . NOTABLE DIFFERENCE ON INDUCING DNA INTERSTRANDCROSS-LINK BETWEEN MUTAGENIC CARCINOGENS ANDNON-CARCINOGENS[J]. Environmental Chemistry, 2001, 20(6): 537-543.
Citation: Ju Xuehai, Zhang Qi, Dai Qianhuan1 . NOTABLE DIFFERENCE ON INDUCING DNA INTERSTRANDCROSS-LINK BETWEEN MUTAGENIC CARCINOGENS ANDNON-CARCINOGENS[J]. Environmental Chemistry, 2001, 20(6): 537-543.
shu

致突变的致癌剂和非致癌剂在引发DNA股间交联上的显著差别

  • 收稿日期:  2001-03-03
基金项目:

国家自然科学基金资助项目(批准号:20042001)

摘要: 借碱洗脱法证明：具有致突变能力的致癌剂1,2-二溴乙烷和肼在经过代谢活化后,均剂量相关地引起L1210细胞中DNA的股间交联。相反,动物致癌试验表现阴性的致突变剂溴乙烷,以及通过各种致癌动物试验均显示阴性的传统常用致突变剂羟胺,在代谢活化以后的同样条件下均不能引起L1210细胞中DNA的股间交联。这证明了双区理论的致癌机理观点,即致癌剂必须是双官能烷化剂,其同时引起互补碱对的交联将引起癌变。相反,股内单一碱基的变异则可能引起致突变作用。并用APCI/SIM(大气压化学电离/选择离子质谱)证明：1,2-二溴乙烷与DNA碱基对的模型反应,与致突实验一致主要引起G-C对的交联和发生G-C→A-T突变。

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