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胸苷激酶缺陷型Friend白血病细胞对丝裂霉素C诱导细胞遗传学畸变的超敏反应。

Hypersensitivity of thymidine kinase-deficient Friend leukaemia cells to the induction of cytogenetic aberrations by mitomycin C.

作者信息

McKenna P G, Yasseen A A

出版信息

Leuk Res. 1985;9(4):501-6. doi: 10.1016/0145-2126(85)90010-4.

DOI:10.1016/0145-2126(85)90010-4
PMID:3923275
Abstract

Clone 707 of the Friend leukaemia cell line was compared with the hypermutable thymidine kinase deficient subclone 707 BUF for sensitivity to the induction of cytogenetic aberrations by mitomycin C (MMC). Two 16-h doses of MMC were utilized, namely 0.1 and 0.15 microgram ml-1. Following removal of MMC from the cultures, metaphase spreads were prepared after 15, 29 and 43 h growth in non-selective medium. Thirteen types of aberrations were scored. The thymidine kinase deficient subclone showed considerably increased sensitivity to the induction of aberrations, with the aberrations also persisting longer. In light of these and earlier reported results, the significance of thymidine kinase for accurate DNA repair is discussed.

摘要

将Friend白血病细胞系的克隆707与高突变的胸苷激酶缺陷亚克隆707 BUF进行比较,以研究丝裂霉素C(MMC)诱导细胞遗传学畸变的敏感性。使用了两剂16小时的MMC,浓度分别为0.1和0.15微克/毫升。从培养物中去除MMC后,在非选择性培养基中生长15、29和43小时后制备中期染色体铺展。对13种类型的畸变进行了评分。胸苷激酶缺陷亚克隆对畸变诱导的敏感性显著增加,且畸变持续时间更长。根据这些结果以及早期报道的结果,讨论了胸苷激酶对准确DNA修复的重要性。

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