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γ射线照射的人淋巴母细胞中DNA损伤的诱导与修复:在有和没有米索硝唑存在的情况下进行照射

Induction and repair of DNA damage in gamma-irradiated human lymphoblasts: irradiation in the presence and absence of misonidazole.

作者信息

Hentosh P

机构信息

Laboratory of Radiobiology, Harvard University School of Public Health, Boston, Massachusetts 02115.

出版信息

Radiat Res. 1988 Sep;115(3):436-47.

PMID:3262883
Abstract

The effects of oxygen and misonidazole on the induction of DNA lesions were examined in human TK6 lymphoblasts irradiated with 60Co gamma rays. We have investigated both the formation and subsequent repair of two classes of DNA damage, single-strand breaks and lesions recognized by the gamma endonuclease activity in a cell-free extract of Micrococcus luteus. Relative to irradiation under hypoxia, single-strand break yields were increased by the presence of either oxygen or misonidazole at the time of irradiation. In contrast, M. luteus enzyme-sensitive site yields were unaffected by the presence of either oxygen or misonidazole. No significant differences in single-strand break or enzyme-sensitive site repair kinetics were observed for lesions induced under any of the irradiation conditions employed. These results confirm the sensitizing effects of oxygen and oxygen-mimetic drugs on the induction of single-strand breaks but provide no support for their ability to enhance the induction of enzyme-sensitive sites.

摘要

在用60Coγ射线照射的人TK6淋巴母细胞中,研究了氧气和米索硝唑对DNA损伤诱导的影响。我们研究了两类DNA损伤的形成及随后的修复情况,即单链断裂和在藤黄微球菌无细胞提取物中由γ核酸内切酶活性识别的损伤。相对于缺氧条件下的照射,照射时氧气或米索硝唑的存在会增加单链断裂的产量。相比之下,藤黄微球菌酶敏感位点的产量不受氧气或米索硝唑存在的影响。在所采用的任何照射条件下诱导产生的损伤,在单链断裂或酶敏感位点修复动力学方面均未观察到显著差异。这些结果证实了氧气和氧模拟药物对单链断裂诱导的增敏作用,但未支持它们增强酶敏感位点诱导的能力。

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