A possible correlation between the growth rate and the extent of DNA damage induced by radiodecay in mouse lymphoma cells.
The extent of DNA single strand breaks resulting from the beta radiodecay of incorporated [3H]thymidine in DNA of mouse lymphoma cells appears to be related to the degree of growth inhibition. The extents of damage to DNA and inhibition of growth seem to be functions of the concentration of radioactivity as well as the specific activity of the radiolabeled precursor in the medium. The differences in both concentration (muCi/ml) and in the specific activity of radiolabeled precursors, may help to explain the different responses encountered when using [3H] and [14C]thymidine. When cells exposed to [3H] TdR are transferred to fresh medium, the DNA damage can be repaired. The repair is followed by an increase in the cell number with the rate of growth being similar to that of unexposed cells. Cells exposed continuously to [3H] TdR in the medium can accommodate to the radioactive stressor by repairing the DNA damage and maintaining this repair capability throughout the exposure.
D000818:Animals; D002455:Cell Division / Q000528:radiation effects; D002460:Cell Line; D002499:Centrifugation, Density Gradient; D004247:DNA / Q000528:radiation effects*; D004260:DNA Repair; D004277:DNA, Single-Stranded / Q000032:analysis; D008223:Lymphoma / Q000235:genetics*; D051379:Mice; D013936:Thymidine / Q000378:metabolism
D004277:DNA, Single-Stranded; D004247:DNA; D013936:Thymidine