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    Modulation of enzyme activity in azaguanine-resistant V79 cells selected by chronic drug exposure.

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    Authors
    Fox, Margaret
    Ockey, C H
    Affiliation
    Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester, M20 9BX, UK.
    Issue Date
    1984-08
    
    Metadata
    Show full item record
    Abstract
    Exposure of V79 cells to azaguanine (7-21 microM for 2-7 weeks) had little effect on growth or plating efficiency but resulted in gradual acquisition of resistance to 8-azaguanine (AZ) and 6-thioguanine (TG) and loss of ability to grow in HAT. The rate of evolution of the resistant phenotype was dependent on the concentration and duration of exposure to AZ. The increase in proportion of resistant cells was paralleled by a rise in phosphatase activity (pH optimum 7.0-7.5) expressed by intact cells and this preceded the fall in HGPRT activity. Elevated phosphatase activity and a resistant phenotype were stably expressed in clones isolated and cultured in the absence of AZ. Hypoxanthine guanine phosphoribosyl transferase (HGPRT) activity in cell extracts of three resistant clones ranged from 18 to 43% of wild-type levels but was unaltered with respect to substrate affinity and electrophoretic mobility. Mg2+-dependent activity dephosphorylated inosine 5'monophosphate (IMP), guanine 5'monophosphate (GMP), adenosine-5-monophosphate (AMP) and p-nitrophenylphosphate (PNPP) and was also elevated with respect to wild-type levels in resistant cell extracts. Purine nucleoside phosphorylase levels were similar in sensitive and resistant cell extracts. Cross-sensitivity studies with other purine analogues suggest that the elevated phosphatase activity does not contribute to the resistant phenotype. No karyotypic changes were observed in the resistant cell lines.
    Citation
    Modulation of enzyme activity in azaguanine-resistant V79 cells selected by chronic drug exposure. 1984, 153 (2):413-24 Exp. Cell Res.
    Journal
    Experimental Cell Research
    URI
    http://hdl.handle.net/10541/123702
    DOI
    10.1016/0014-4827(84)90610-4
    PubMed ID
    6329796
    Type
    Article
    Language
    en
    ISSN
    0014-4827
    ae974a485f413a2113503eed53cd6c53
    10.1016/0014-4827(84)90610-4
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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