DNA excision repair as a component of adaptation to low doses of ionizing radiation in Escherichia coli.
DNA excision repair as a component of adaptation to low doses of ionizing radiation in Escherichia coli.
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DNA 切除修复是大肠杆菌适应低剂量电离辐射的一个组成部分。
DOI：
10.1080/09553009314551831
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发表时间：
1993
影响因子：
2.6
通讯作者：
Claycamp,HG
中科院分区：
文献类型：
--
作者：
Huang,H;Claycamp,HG
在这项研究中，我们检查了DNA切除修复是否是大肠杆菌（一种特征良好的原核生物）中由极低剂量电离辐射诱导的适应的组成部分，并研究了增强的切除修复与SOS反应之间的关系。有能力E.使用低剂量（0·1–10 Gy）的 137 Cs γ 射线照射大肠杆菌细胞，使其恢复 2 小时，然后使用每分子含有约 22 个氧化胸腺嘧啶残基（胸腺嘧啶二醇）的 pUC18 DNA 进行转化。通过恢复质粒携带的氨苄青霉素抗性来鉴定成功的转化体，并使用所得数据（菌落计数）来计算受辐射细胞与对照细胞中质粒恢复的比率。结果表明，接受极低剂量 (0·1–0·5 Gy) 照射的细胞利用含胸腺嘧啶乙二醇的 pUC18 DNA 的效率提高了 30–40%。在使用recA细胞或携带recA-lacZ基因融合的细胞的实验中，极低剂量（<0·5Gy）γ射线增强的切除修复被证明与recA控制的SOS反应无关。随后使用 DNA 沉淀测定证实了 AB1157 原型细胞中的刺激效果，其中通过用溴化乙锭抑制 DNA 连接来累积 DNA 切割事件。我们的数据表明，诱导不依赖于 SOS 的 DNA 切除修复的剂量效应似乎存在狭窄的“窗口”。与哺乳动物细胞研究类似，这种效应的剂量范围比 D37 辐射存活的剂量范围小约 200 倍。
In this study we examined whether or not DNA excision repair is a component of adaptation induced by very low-dose ionizing radiation inEscherichia coli, a well-characterized prokaryote, and investigated the relationship between enhanced excision repair and the SOS response. CompetentE. colicells were irradiated using low doses (0·1–10 Gy) of137Cs γ-rays, allowed to recover for 2 h and were then transformed using pUC18 DNA containing approximately 22 oxidized thymine residues (thymine glycols) per molecule. Successful transformants were identified by recovery of plasmid-borne ampicillin resistance and the resulting data (colony counts) were used to calculate ratios of plasmid recovery in irradiated to control cells. Results showed that cells irradiated with very low doses (0·1–0·5 Gy) were up to 30–40% more efficient at utilizing thymine glycol-containing pUC18 DNA. The enhanced excision repair by very low doses (< 0·5 Gy) of γ-rays was shown to be independent of therecA-controlled SOS response in experiments usingrecA cells or cells carryingrecA-lacZ gene fusions. The stimulating effect in AB1157 prototype cells were subsequently confirmed using a DNA precipitation assay in which DNA incision events were accumulated by inhibiting DNA ligation with ethidium bromide. Our data suggest that there seems to be narrow ‘windows’ of dose—effect for the induction of SOS-independent DNA excision repair. Being similar to mammalian cell studies, the dose range for this effect was about 200-fold less thanD37for radiation survival.
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影响因子：
2.6
作者：
Shadley,JD;Wiencke,JK
通讯作者：
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DOI：
10.1080/09553007814550491
发表时间：
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期刊：
International journal of radiation biology and related studies in physics, chemistry, and medicine
影响因子：
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作者：
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DOI：
10.1016/0921-8777(90)90065-d
发表时间：
1990
期刊：
Mutation research
影响因子：
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作者：
F. Darroudi;A. Natarajan;G. P. van der Schans;A. A. van Loon
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A. A. van Loon
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影响因子：
64.8
作者：
B. Miletić;Ž. Kućan;D. Novak
通讯作者：
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影响因子：
2.6
作者：
LIU, SZ;CAI, L;SUN, SQ
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SUN, SQ