Cohen M M, Simpson S J
Environ Mutagen. 1982;4(1):27-36. doi: 10.1002/em.2860040105.
Bleomycin, a radiomimetic glycopeptide, inhibits de novo DNA synthesis in ataxia telangiectasia lymphoblastoid B cells to a markedly lesser extent than in normal and xeroderma pigmentosum lymphoid cells. This observation is similar to that following ionizing radiation; however, the effect is slower following the chemical treatment. Recovery of the normal cells occurs 15-18 hours after treatment, whereas the ataxia telangiectasia lines do not attain normal levels of DNA synthesis during the entire 24-hour observation period. Similar differences were not observed following treatment with mitomycin C, a bifunctional alkylating agent, indicating a specific effect of bleomycin on DNA synthesis in ataxia telangiectasia cells. Following bleomycin treatment and preincubation with hydroxyurea, residual DNA synthesis in ataxia telangiectasia cells was similar to that in both normal and xeroderma pigmentosum lymphoid cells, suggesting that the capacity to repair the induced DNA lesion is present.
博来霉素是一种拟放射糖肽，与正常淋巴细胞和着色性干皮病淋巴细胞相比，它对共济失调毛细血管扩张症淋巴母细胞样B细胞中DNA从头合成的抑制作用明显较弱。这一观察结果与电离辐射后的情况相似；然而，化学处理后的效应较慢。正常细胞在处理后15 - 18小时恢复，而共济失调毛细血管扩张症细胞系在整个24小时观察期内未达到正常的DNA合成水平。用丝裂霉素C（一种双功能烷化剂）处理后未观察到类似差异，这表明博来霉素对共济失调毛细血管扩张症细胞中的DNA合成有特定作用。在博来霉素处理并与羟基脲预孵育后，共济失调毛细血管扩张症细胞中的残余DNA合成与正常淋巴细胞和着色性干皮病淋巴细胞中的相似，这表明存在修复诱导性DNA损伤的能力。
