Mutagen sensitivity in thymidine kinase- and methyltransferase-deficient human lymphoblastoid cells

CJ Best, PG McKenna, Valerie McKelvey-Martin

    Research output: Contribution to journalArticle

    Abstract

    In this study the effect of thymidine kinase deficiency on the responses of the human lymphoblastoid cell line Raji to methyl methanesulphonate and mitomycin C was investigated. Mutagen sensitivity was measured in terms of cell survival and mutation to hypoxanthine-guanine phosphoribosyltransferase deficiency. Thymidine kinase-deficient Raji cells showed decreased survival and increased mutant frequency relative to wild-type cells following treatments with each of the mutagens used. It is suggested that this may be due to an imbalance in the supply of deoxyribonucleoside triphosphates to the excision repair process. The role of O-6-methylguanine-DNA methyltransferase in the repair of DNA damage caused by these mutagens is also discussed.
    LanguageEnglish
    Pages267-272
    JournalBritish Journal of Biomedical Science
    Volume54
    Issue number4
    Publication statusPublished - Dec 1997

    Fingerprint

    Thymidine Kinase
    Mutagens
    Methyltransferases
    O(6)-Methylguanine-DNA Methyltransferase
    Lesch-Nyhan Syndrome
    Deoxyribonucleosides
    Methyl Methanesulfonate
    Mitomycin
    DNA Repair
    DNA Damage
    Cell Survival
    Cell Line
    Mutation
    Survival

    Cite this

    Best, CJ ; McKenna, PG ; McKelvey-Martin, Valerie. / Mutagen sensitivity in thymidine kinase- and methyltransferase-deficient human lymphoblastoid cells. In: British Journal of Biomedical Science. 1997 ; Vol. 54, No. 4. pp. 267-272.
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    abstract = "In this study the effect of thymidine kinase deficiency on the responses of the human lymphoblastoid cell line Raji to methyl methanesulphonate and mitomycin C was investigated. Mutagen sensitivity was measured in terms of cell survival and mutation to hypoxanthine-guanine phosphoribosyltransferase deficiency. Thymidine kinase-deficient Raji cells showed decreased survival and increased mutant frequency relative to wild-type cells following treatments with each of the mutagens used. It is suggested that this may be due to an imbalance in the supply of deoxyribonucleoside triphosphates to the excision repair process. The role of O-6-methylguanine-DNA methyltransferase in the repair of DNA damage caused by these mutagens is also discussed.",
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    Mutagen sensitivity in thymidine kinase- and methyltransferase-deficient human lymphoblastoid cells. / Best, CJ; McKenna, PG; McKelvey-Martin, Valerie.

    In: British Journal of Biomedical Science, Vol. 54, No. 4, 12.1997, p. 267-272.

    Research output: Contribution to journalArticle

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    AU - Best, CJ

    AU - McKenna, PG

    AU - McKelvey-Martin, Valerie

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    AB - In this study the effect of thymidine kinase deficiency on the responses of the human lymphoblastoid cell line Raji to methyl methanesulphonate and mitomycin C was investigated. Mutagen sensitivity was measured in terms of cell survival and mutation to hypoxanthine-guanine phosphoribosyltransferase deficiency. Thymidine kinase-deficient Raji cells showed decreased survival and increased mutant frequency relative to wild-type cells following treatments with each of the mutagens used. It is suggested that this may be due to an imbalance in the supply of deoxyribonucleoside triphosphates to the excision repair process. The role of O-6-methylguanine-DNA methyltransferase in the repair of DNA damage caused by these mutagens is also discussed.

    M3 - Article

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