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首页> 外文期刊>日本兽医学杂誌 >Induction of fragile sites by fluorodeoxyuridine and caffeine accompanies with misincorpolation of exogenous uridine nucleotide into DNA of feline fibroblasts
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Induction of fragile sites by fluorodeoxyuridine and caffeine accompanies with misincorpolation of exogenous uridine nucleotide into DNA of feline fibroblasts

机译：氟脱氧尿苷和咖啡因诱导脆性位点伴随着外源尿苷核苷酸误掺入猫成纤维细胞DNA中

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Fluorodeoxyuridine, an inhibitor of thymidylate synthetase, is known to induce chromosomal fragile sites. The drug treatment may cause deprivation of intracellular thymidine nucleotide pool followed by a serious imbalance of deoxynucleotide pool. Though the stress is probably related to the induction of folate-sensitive fragile sites, the exact machanism is still to be investigated. The present study has been carried out to test the possibility that the fragile sites are originated, at least in part, from incorpolated uracil residues. The incorpolated uracil residue can be detected by a novel assay for abasic sites after treatment with uracil-DNA N-glycosylase (UDG). About 2.7 abasic sites per 10~4 nucleotides were detected in the DNA extracted from feline fibroblasts after the treatment with FUdR and caffeine. By digesting the DNA with UDG prior to the assay, significant increase in the number of abasic sites were observed. These results indicate that the large amount of uracil residues are present in the feline fibroblast DNA under the condition which induces chromosomal fragile sites.
机译：已知胸苷酸合成酶的抑制剂氟脱氧尿苷可诱导染色体易碎位点。药物治疗可能会导致细胞内胸腺嘧啶核苷池被剥夺，继而导致脱氧核苷酸池严重失衡。尽管应力可能与叶酸敏感的脆弱部位的诱导有关，但确切的机理尚待研究。进行本研究以测试易碎部位至少部分源自掺入的尿嘧啶残基的可能性。掺入的尿嘧啶残基可以在用尿嘧啶-DNA N-糖基化酶（UDG）处理后通过针对无碱基位点的新颖测定来检测。经FUdR和咖啡因处理后，从猫成纤维细胞提取的DNA中，每10〜4个核苷酸中大约有2.7个脱碱基位点。通过在测定之前用UDG消化DNA，可以观察到无碱基位点数量的显着增加。这些结果表明，在诱导染色体易碎位点的条件下，猫成纤维细胞DNA中存在大量尿嘧啶残基。

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