Cohen M M, Simpson S J
Mutat Res. 1983 Apr;112(2):119-28. doi: 10.1016/0167-8817(83)90016-0.
Cytogenetic damage in cells cultured from normal individuals and patients with ataxia telangiectasia (A-T) and xeroderma pigmentosum (XP) was induced by the chemotherapeutic antibiotics neocarzinostatin (NCS), tallysomycin (TLM) and bleomycin (BLM). Chromosomal breakage was specifically elevated in A-T cells when compared to the other genotypes tested. Similar results were not observed with the clastogens mitomycin C (MMC) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as all cells responded similarly. All 5 chemical agents caused a marked suppression of de novo DNA synthesis in normal and XP long-term lymphoid cell lines while the A-T cells seemed resistant to this effect of NCS, TLM and BLM.
用化疗抗生素新制癌菌素（NCS）、 tallysomycin（TLM）和博来霉素（BLM）诱导正常个体以及共济失调毛细血管扩张症（A-T）和着色性干皮病（XP）患者培养的细胞发生细胞遗传学损伤。与其他受试基因型相比，A-T细胞中的染色体断裂明显增加。用丝裂霉素C（MMC）和N-甲基-N'-硝基-N-亚硝基胍（MNNG）等致断裂剂未观察到类似结果，因为所有细胞的反应相似。所有5种化学试剂均显著抑制正常和XP长期淋巴细胞系中的DNA从头合成，而A-T细胞似乎对NCS、TLM和BLM的这种作用具有抗性。
