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Imidazole Ring-Opened DNA Purines and Their Biological Significance
Tudek, Barbara 한국생화학분자생물학회 2003 BMB Reports Vol.36 No.1
Fragmentation of purine imidazole ring and production of formamidopyrimklines in deoxynucleosides (Fapy lesions) occurs upon DNA oxidation as well as upon spontaneous or alkali-triggered rearrangement of certain alkylated bases. Many chemotherapeutic agents alkylated bases. Many chemotherapeutic agents such as cyclophosphamide or thiotepa produce such lesions in DNA. Unsubstitued Fapy A and Fapy G, Formed upon DNA oxidation cause moderate inhibition of DNA synthesis, which is DNA polymerase and sequence dependent. Fapy-7MeG, a methylated counterpart of Fapy-G-, a efficiently inhibits DNA replication in vitro and in E,coli, however its mutagenic potency is low. This is porbably due to preferential incorporation of cytosine opposite Fapy-7MeG and preferential extension of Fapy-7MeG : C pair. In contrast, Fapy A and Fapy-7MeG possess miscoding potential. Both lesions in SOS induced E.coli preferentially mispair with cytosine giving rise to A→G transitions. Fapy lesions substituted with longer chain alkyl groups also show are actively eliminated from DNA by repair glycosylases specific for oxidized purines and pyrimidines both in bacteria and eukaryotic cells. Baterial enzymes include E.coli formamidopyrimidine-DNA-glycosylase (Fpg protein), endonuclease Ⅲ (Nth protein) and endonuclease Ⅷ (Nei protein).
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Imidazole Ring-Opened DNA Purines and Their Biological Significance
Barbara, Tudek Korean Society for Biochemistry and Molecular Biol 2003 Journal of biochemistry and molecular biology Vol.36 No.1
Fragmentation of purine imidazole ring and production of formamidopyrimidines in deoxynucleosides (Fapy lesions) occurs upon DNA oxidation as well as upon spontaneous or alkali-triggered rearrangement of certain alkylated bases. Many chemotherapeutic agents such as cyclophosphamide or thiotepa produce such lesions in DNA. Unsubstituted FapyA and FapyG, formed upon DNA oxidation cause moderate inhibition of DNA synthesis, which is DNA polymerase and sequence dependent. Fapy-7MeG, a methylated counterpart of FapyG-, a efficiently inhibits DNA replication in vitro and in E.coli, however its mutagenic potency is low. This is probably due to preferential incorporation of cytosine opposite Fapy-7MeG and preferential extension of Fapy-7MeG:C pair. In contrast, FapyA and Fapy-7MeA possess miscoding potential. Both lesions in SOS induced E.coli preferentially mispair with cytosine giving rise to A$\rightarrow$G transitions. Fapy lesions substituted with longer chain alkyl groups also show simult aneous lethal and mutagenic properties. Fapy lesions are actively eliminated from DNA by repair glycosylases specific for oxidized purines and pyrimidines both in bacteria and eukaryotic cells. Bacterial enzymes include E.coli formamidopyrimidine-DNA-glycosylase (Fpg protein), endonuclease III (Nth protein) and endonuclease VIII (Nei protein).
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