Rapidly occurring DNA excision repair events determine the biological expression of u.v.-induced damage in human cells
- 1 September 1987
- journal article
- research article
- Published by Oxford University Press (OUP) in Carcinogenesis: Integrative Cancer Research
- Vol. 8 (9), 1251-1256
- https://doi.org/10.1093/carcin/8.9.1251
Abstract
We have developed a new assay which allows us to monitor the rates of repair of potentially lethal damage in u.v. (254 nm)-irradiated normal human skin fibroblasts. Using this assay we have shown that, in non-dividing cells, the majority of biologically effective excision repair is completed within 4 h following irradiation with low fluences of u.v. (1.5–6.0 J/m 2 ). During this time, non-dividing cells removed only ∼20% of the pyrimidine dimers induced in DNA by a u.v. fluence of 3.0 J/m 2 as measured by the loss of u.v.-endonuclease-sensitive sites under identical repair conditions. The rates of repair of potentially lethal damage were also found to be independent of u.v. fluence over the range 1.5–6.0 J/m 2 in non-dividing cells. In contrast, in cells irradiated in exponential growth with 1.5 J/m 2 , the rate of biologically effective repair was comparable with that observed in non-dividing cells but the efficiency of the repair process declined progressively with increase in u.v. fluence from 1.5 to 6.0 J/m 2 . Our data support the concept that the biological recovery of u.v.-irradiated cells depends on the preferential repair of damage in functionally important domains in the genome.This publication has 2 references indexed in Scilit:
- Survival of UV-irradiated mammalian cells correlates with efficient DNA repair in an essential gene.Proceedings of the National Academy of Sciences, 1986
- DNA repair and survival in UV-irradiated chicken embryo fibroblastsMutation Research, 1980