You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Effect of Arabinofuranosyladenine on Radiation-Induced Chromosome Damage in Plateau-Phase CHO Cells Measured by Premature Chromosome Condensation: Implications for Repair and Fixation of α-PLD
George Iliakis, Gabriel E. Pantelias and Robert Seaner
Vol. 114, No. 2 (May, 1988), pp. 361-378
Published by: Radiation Research Society
Stable URL: http://www.jstor.org/stable/3577231
Page Count: 18
You can always find the topics here!Topics: Chromosomes, CHO cells, Radiation damage, DNA damage, Cell lines, HeLa cells, Cell culture techniques, Incubation, Cultured cells, Irradiation
Were these topics helpful?See somethings inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
The effect of the DNA polymerase inhibitor β-arabinofuranosyladenine (araA) on radiation-induced damage was studied at the cell survival and chromosome level in unfed plateau-phase cultures of Chinese hamster ovary cells. At the cell survival level postirradiation treatment with araA fixed a form of radiation-induced potentially lethal damage, termed α-PLD. In the absence of araA treatment, repair of PLD resulted in the formation of the survival curve shoulder in immediately plated cells and in the increase in survival observed after delayed plating. The repair kinetics observed after delayed plating of plateau-phase cells or after delayed administration of 500 μM araA were similar, suggesting that both protocols assay similar lesions. AraA-mediated fixation reached a plateau at concentrations higher than 500 μM, indicating complete fixation of α-PLD. At the cytogenetic level, postirradiation treatment with araA at concentrations higher than 500 μM caused a complete inhibition of chromosome repair, as scored by premature chromosome condensation. In the absence of araA, the linearity of the dose-effect relationship for chromosome fragmentation obtained immediately after irradiation was preserved even after long repair times. The repair kinetics of chromosome damage measured in cells held postirradiation in the plateau phase were the mirror image of the repair kinetics for α-PLD. The half-time was 1 h in both cases and repair reached a plateau after about 4-6 h. AraA-mediated repair inhibition of chromosome damage was reversible, and a decrease in residual chromosome damage was observed after post-treatment incubation in araA-free conditioned medium. This persistent chromosome damage increased with increasing araA concentration and, as with PLD fixation, reached a plateau at about 500 μM. These results suggest that repair and araA-mediated fixation of α-PLD have their counterparts at the chromosome level as indicated by the similar repair kinetics and inhibition/fixation characteristics obtained for α-PLD and chromosome damage. This relationship implies a correlation between repair at the DNA and the chromosome level and suggests that DNA polymerization is required for the repair of chromosome damage.
Radiation Research © 1988 Radiation Research Society