Journal
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
Volume 77, Issue 12, Pages 1163-1174Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/09553000110086372
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Purpose : To analyse the relationship between radiation-induced clonogenic cell death, chromosome aberrations and markers of proliferative senescence or differentiation. Materials and methods : Plateau-phase human dermal fibroblasts from 18 donors were irradiated with graded doses of 1-6 Gy 200 kV X-rays. Cell survival was determined by a colony-forming assay. Markers of differentiation or senescence were: spontaneous and radiation-induced clonal differentiation, which was determined morphologically and by the cellular potential to proliferate in clonal culture, also single-cell beta -galactosidase (beta -gal) staining at pH 6.0; and the secretion of transforming growth factor-beta (TGF-beta1) into the culture medium. Chromosome aberrations were determined as genomic yields of dicentric chromosomes and the excess acentric fragments, scored in Giemsa-stained metaphases, and as partial yields of reciprocal translocations for chromosomes 4, 7 and 9 using the FISH method. Results: A broad spread was found in the shapes of the survival curves, with SF2 ranging from 0.041 +/- 0.015 to 0.63 +/- 0.05. Radiation-induced clonal differentiation as well as the secretion of TGF-beta1 was elevated in radiosensitive samples. With respect to chromosome aberrations, a significant correlation was found between clonogenic survival and radiation-induced excess acentric fragments. Conclusions : In the fibroblast cell system, in vitro radiosensitivity is determined not only by processes directly involved in DNA-damage recognition and repair, but also by intracellular signalling cascades, which will lead to differentiation processes.
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