Long-term repair in vivo of colony-forming ability and chromosomal injury in X-irradiated mouse hepatocytes.
The radiosensitivity of mouse hepatocytes in vivo was measured in terms of clonogenicity or chromosome damage (micronucleus production). Within 24 h of irradiation there was a dose-dependent increase in clonogenicity (dose-modifying factor, DMF = 1.37 +/- 0.09) followed by long-term repair which resulted in a DMF of 3.49 +/- 0.23 at 11 months. Such repair also took place, but to a lesser extent, after the end of fractionated irradiation. Cell proliferation, measured by tritiated thymidine autoradiography, was insufficient to explain the long-term reduction in radiosensitivity in terms of a dose-dependent replacement of damaged cells. Although there was a reduction in the frequency of cells with micronuclei, postirradiation, the magnitude of this decrease was relatively small; the DMF for micronucleus-free cells at 11 months was only 1.49 +/- 0.25. Thus the long-term increase in clonogenicity can only partially be explained in terms of repair of chromosome injury, assessed by the production of micronuclei.
Fisher
D R
DR
Department of Radiobiology, Paterson Institute for Cancer Research, Christie Hospital and Holt Radium Institute, Manchester, United Kingdom.
Hendry
J H
JH
Scott
D
D
D000818:Animals; D002470:Cell Survival / Q000528:radiation effects; D002869:Chromosome Aberrations; D004260:DNA Repair; D008099:Liver / Q000166:cytology / Q000528:radiation effects*; D051379:Mice; D013234:Stem Cells / Q000528:radiation effects*; D013997:Time Factors