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. 1999 Jan 1;108(1):38-41.
doi: 10.1016/s0165-4608(98)00108-3.

The contribution of deficient DNA repair to chromosomal radiosensitivity of CHO cells after G2 irradiation

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The contribution of deficient DNA repair to chromosomal radiosensitivity of CHO cells after G2 irradiation

K K Sanford et al. Cancer Genet Cytogenet. .

Abstract

We compared cytogenetic responses of the parental Chinese hamster ovary (CHO) cell line and its DNA repair-deficient strains to irradiation during the G2 phase. Chromatid breaks were quantified in cells entering metaphase in the presence or absence of cytosine arabinoside (ara-C) 0.5-1.5 hours after exposure to x-rays or UV-C. Addition of ara-C, an inhibitor of DNA repair replication, significantly increased chromatid break frequency (CBF) in the parental line, but not in the strains deficient in nucleotide excision repair (NER). This increase (ara-C effect) was comparable to that in repair-proficient normal human lymphocytes. We conclude that CBF in cells entering metaphase in the presence of ara-C 0.5-1.5 hours after DNA damage represents a functional in vitro assay for evaluating the DNA repair capacity of mammalian cells in culture.

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