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Multiple Mechanisms of Adenosine Toxicity in an Adenosine Sensitive Mutant of Baby Hamster Kidney (BHK) Cells

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Genetic Consequences of Nucleotide Pool Imbalance

Part of the book series: Basic Life Sciences ((BLSC,volume 31))

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Abstract

A class of arabinosyladenine-resistant baby hamster kidney (BHK) cell mutants, isolated in our laboratory, shows cross-resistance to deoxyadenosine, alteration of adenosine kinase, elevation of spontaneous mutation rate, and extreme sensitivity to adenosine. One of these adenosine sensitive mutants, ara-slOd, was isolated spontaneously and studies with Ador revertants suggest the involvement of a single pleiotropic mutation. The enhanced adenosine toxicity in ara-slOd cells can be attributed to pyrimidine nucleotide starvation and to at least one other mechanism, which is associated with a 200-fold elevation of IMP, 3–5 fold elevation of ATP, GTP, S-adeno- sylmethionine (AdoMet) and methylthioadenosine (MeSAdo).

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© 1985 Plenum Press, New York

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Chan, VL., Ho, H.J. (1985). Multiple Mechanisms of Adenosine Toxicity in an Adenosine Sensitive Mutant of Baby Hamster Kidney (BHK) Cells. In: de Serres, F.J. (eds) Genetic Consequences of Nucleotide Pool Imbalance. Basic Life Sciences, vol 31. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2449-2_6

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  • DOI: https://doi.org/10.1007/978-1-4613-2449-2_6

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-9488-7

  • Online ISBN: 978-1-4613-2449-2

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