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.
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Research Article| January 01 1988
Long-Term Repair in Vivo of Colony-Forming Ability and Chromosomal Injury in X-Irradiated Mouse Hepatocytes
Radiat Res (1988) 113 (1): 40–50.
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D. R. Fisher, J. H. Hendry, D. Scott; Long-Term Repair in Vivo of Colony-Forming Ability and Chromosomal Injury in X-Irradiated Mouse Hepatocytes. Radiat Res 1 January 1988; 113 (1): 40–50. doi: https://doi.org/10.2307/3577178
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