Somatic Cell Genetics

, Volume 4, Issue 5, pp 587–601

Biological and biochemical effects of bromodeoxyuridine and deoxycytidine on Syrian hamster melanoma cells

  • Elliot R. Kaufman
  • Richard L. Davidson
Article

DOI: 10.1007/BF01542928

Cite this article as:
Kaufman, E.R. & Davidson, R.L. Somat Cell Mol Genet (1978) 4: 587. doi:10.1007/BF01542928

Abstract

The addition of deoxycytidine (dCyd) to the growth medium of cultured Syrian hamster melanoma cells causes a reversal of the toxic effects of 5-bromodeoxyuridine (BrdU) and a decrease in the extent of incorporation of BrdU into nuclear DNA. These effects of dCyd can be accounted for, in part, by the intracellular conversion of the exogenously supplied dCyd to thymidine (dThd) nucleotides which can compete with BrdU nucleotides for incorporation into DNA. To some extent, the conversion of dCyd to dThd nucleotides can be inhibited by increasing the concentration of BrdU in the growth medium. The conversion of dCyd to dThd nucleotides is inhibited completely by aminopterin (Apt), and Apt also prevents dCyd from reversing BrdU toxicity and from decreasing the level of BrdU incorporation into nuclear DNA. In a clone of Syrian hamster melanoma cells, increasing the concentration of dCyd in the growth medium from 1 μM to 1000 μM resulted in a progressive increase in the percentage of dThd residues in nuclear DNA being derived from the exogenous dCyd, until more than 90% of the dThd residues came from the exogenous dCyd. However, despite the increasing amount of dThd derived from exogenous dCyd, there was a plateau in the decrease in BrdU incorporation into nuclear DNA at concentrations of dCyd above 8 μM.

Copyright information

© Plenum Publishing Corporation 1978

Authors and Affiliations

  • Elliot R. Kaufman
    • 1
    • 2
  • Richard L. Davidson
    • 1
    • 2
  1. 1.Division of Human GeneticsChildren's Hospital Medical CenterUSA
  2. 2.Department of Microbiology and Molecular GeneticsHarvard Medical SchoolBoston

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