Association of poly(adenosine diphosphoribose) synthesis with DNA damage and repair in normal human lymphocytes.
Association of poly(adenosine diphosphoribose) synthesis with DNA damage and repair in normal human lymphocytes.
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正常人淋巴细胞中聚（腺苷二磷酸核糖）合成与 DNA 损伤和修复的关联。
DOI：
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发表时间：
1979
影响因子：
15.9
通讯作者：
Kevin K. Kurohara
中科院分区：
文献类型：
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作者：
N. Berger;G. W. Sikorski;S. Petzold;Kevin K. Kurohara
用通透性细胞技术检测不同类型DNA损伤剂对正常人淋巴细胞DNA和多聚(二磷酸腺苷)合成的影响。在紫外线(UV)照射下，淋巴细胞的DNA和多聚(腺苷二磷酸核糖)的非程序合成突然增加。照射后1h内明显升高，照射后2~4h达最大。DNA和多聚(腺苷二磷酸核糖)合成增加的幅度取决于紫外线剂量。用DNA的溴脱氧尿嘧啶核苷密度标记的碱性CsC l梯度研究表明，DNA合成的非程序合成实际上是DNA合成修复模式的结果。当淋巴细胞被其他几种DNA损伤剂处理时，DNA合成和多聚(二磷酸腺苷)合成也有类似的增加，包括博莱霉素、N-甲基-N‘-硝基-N-亚硝基-N-亚硝基或N-乙氧基乙酰氨基荧光烯。在允许细胞DNA降解的条件下，用DNA酶处理淋巴细胞，也可以增加多聚(腺苷二磷酸核糖)的合成。放线菌亚胺不能抑制DNA或多聚(腺苷二磷酸核糖)合成的增加，这种增加是由DNA损伤剂处理引起的。
A permeable cell technique was used to measure the alterations in synthesis of DNA and poly-(adenosine diphosphoribose) in normal human lymphocytes after treatment of the cells with different types of DNA-damaging agents. The lymphocytes showed an abrupt increase in the unscheduled synthesis of DNA and poly(adenosine diphosphoribose) in response to ultraviolet (UV) irradiation. The increases were apparent within 1 h and reached a maximum between 2 and 4 h after irradiation. The magnitude of the increases in DNA and poly(adenosine diphosphoribose) synthesis was dependent upon the UV dose. Alkaline CsCl gradient studies, with bromodeoxyuridine triphosphate density labeling of DNA, demonstrated that the unscheduled DNA synthesis, which occurred in response to UV irradiation, was actually a result of the repair mode of DNA synthesis. Similar increases in DNA synthesis, and poly(adenosine diphosphoribose) synthesis occurred when lymphocytes were treated with several other DNA-damaging agents, including bleomycin, N-methyl-N'-nitro-N-nitrosoguanidine or N-acetoxyacetyl aminofluorene. Treatment of lymphocytes with DNase, under conditions which allowed degradation of cellular DNA, also resulted in increased synthesis of poly(adenosine diphosphoribose). Cycloheximide did not inhibit the increase in synthesis of DNA or poly(adenosine diphosphoribose) that occurred in response to treatment with the DNA-damaging agents.