Sanford K K, Parshad R
Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland, USA.
Cancer Genet Cytogenet. 1999 Jan 1;108(1):38-41. doi: 10.1016/s0165-4608(98)00108-3.
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.
我们比较了亲代中国仓鼠卵巢（CHO）细胞系及其DNA修复缺陷型菌株在G2期对辐射的细胞遗传学反应。在暴露于X射线或UV-C后0.5 - 1.5小时，在有或无胞嘧啶阿拉伯糖苷（ara-C）的情况下，对进入中期的细胞中的染色单体断裂进行定量。DNA修复复制抑制剂ara-C的添加显著增加了亲代细胞系中的染色单体断裂频率（CBF），但在核苷酸切除修复（NER）缺陷的菌株中未增加。这种增加（ara-C效应）与修复功能正常的正常人淋巴细胞中的增加相当。我们得出结论，在DNA损伤后0.5 - 1.5小时存在ara-C的情况下进入中期的细胞中的CBF代表了一种用于评估培养的哺乳动物细胞DNA修复能力的功能性体外试验。
