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    Role of nucleotide excision repair in processing of O4-alkylthymines in human cells.

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    Authors
    Klein, J C
    Bleeker, M J
    Roelen, H C
    Rafferty, Joseph A
    Margison, Geoffrey P
    Brugghe, H F
    Van den Elst, H
    Van der Marel, G A
    Van Boom, J H
    Kriek, E
    Affiliation
    Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam.
    Issue Date
    1994-10-14
    
    Metadata
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    Abstract
    O4-Alkylthymines have been implicated as potential carcinogenic DNA lesions. We have studied the effects of O4-methylthymine, O4-ethylthymine, and O4-n-propylthymine in a model system in which a single lesion was located at a defined position on a SV40-based shuttle vector and have found large differences in the effects of these lesions in repair-proficient and nucleotide excision repair-deficient cells. In repair-competent human HeLa cells, normal fibroblasts, and XP-A (2OS) revertant cells, all 3 residues were highly mutagenic; a mutation frequency of approximately 20% was found for both O4-methylthymine and O4-ethylthymine, whereas that of O4-n-propylthymine was approximately 12%. These frequencies were independent of the activity of the O6-alkylguanine DNA alkyltransferase. All three O4-alkylthymines induced T-->C transitions exclusively. In nucleotide excision repair-deficient XP-A cells, however, these lesions were not mutagenic but strongly inhibited plasmid replication (> 90%). These results indicate that O4-alkylthymines are efficiently recognized by the nucleotide excision repair system and cause a complete cessation of plasmid replication if this system is deficient. Nevertheless, proficiency in the nucleotide excision repair pathway correlates with a high frequency of mutation induction by these lesions.
    Citation
    Role of nucleotide excision repair in processing of O4-alkylthymines in human cells. 1994, 269 (41):25521-8 J. Biol. Chem.
    Journal
    The Journal of Biological chemistry
    URI
    http://hdl.handle.net/10541/96108
    PubMed ID
    7929253
    Type
    Article
    Language
    en
    ISSN
    0021-9258
    Collections
    All Paterson Institute for Cancer Research

    entitlement

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