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着色性干皮病细胞中γ射线诱导的DNA损伤修复缺陷。

Defective repair of gamma-ray induced DNA damage in xeroderma pigmentosum cells.

作者信息

Setlow R B, Faulcon F M, Regan J D

出版信息

Int J Radiat Biol Relat Stud Phys Chem Med. 1976 Feb;29(2):125-36. doi: 10.1080/09553007614550141.

DOI:10.1080/09553007614550141
PMID:1083379
Abstract

We used the bromouracil-photolysis technique to estimate the sizes of the repaired regions in normal human and xeroderma pigmentosum (XP) cells irradiated by gamma-rays aerobically or anoxically. After 1 1/2 hours of incubation, single-strand breaks were repaired and the repaired regions were small--one to two BrUra residues--for cells irradiated aerobically or anoxically. After a 20-hour incubation, the repaired region in normal cells showed a component mimicking U.V.-repair. There were large patches (approximately 30 BrUra residues) in the approximate ratios of one per six chain breaks for aerobic irradiation and one per three chain breaks for anoxic irradiation. XP cells, however, only showed large patches at 20 hours if they had been irradiated aerobically. We could not detect such regions in XP cells irradiated anoxically. These results indicate (1) that some part of ionizing damage mimics excision of U.V. damage in that the repair patches are large and the repair takes an appreciable time; (2) the types of such damage depend on whether the irradiation is done aerobically or anoxically; and (3) XP cells are defective in repairing a component of anoxic damage.

摘要

我们使用溴尿嘧啶光解技术来估计在需氧或厌氧条件下受到γ射线照射的正常人细胞和着色性干皮病(XP)细胞中修复区域的大小。孵育1.5小时后,单链断裂得到修复,对于需氧或厌氧照射的细胞,修复区域较小,为一到两个溴尿嘧啶残基。孵育20小时后,正常细胞中的修复区域显示出一种模拟紫外线修复的成分。对于需氧照射,有大片段(约30个溴尿嘧啶残基),其比例约为每六个链断裂中有一个;对于厌氧照射,比例约为每三个链断裂中有一个。然而,XP细胞只有在需氧照射后20小时才会出现大片段。在厌氧照射的XP细胞中我们检测不到这样的区域。这些结果表明:(1)电离损伤的某些部分模拟了紫外线损伤的切除,因为修复片段大且修复需要相当长的时间;(2)这种损伤的类型取决于照射是在需氧还是厌氧条件下进行;(3)XP细胞在修复厌氧损伤的一个成分方面存在缺陷。

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引用本文的文献

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DNA excision-repair defect of xeroderma pigmentosum prevents removal of a class of oxygen free radical-induced base lesions.着色性干皮病的DNA切除修复缺陷会阻止一类氧自由基诱导的碱基损伤的去除。
Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6335-9. doi: 10.1073/pnas.90.13.6335.
2
Cross-sensitivity of certain xeroderma pigmentosum and Cockayne syndrome fibroblast strains to both ionizing radiation and ultraviolet light.某些着色性干皮病和成骨不全综合征成纤维细胞株对电离辐射和紫外线的交叉敏感性。
Mol Gen Genet. 1981;181(4):562-3. doi: 10.1007/BF00428755.
3
The combined action of chemical carcinogens on DNA repair in human cells.
Radiat Environ Biophys. 1980;18(1):57-64. doi: 10.1007/BF01324374.
4
Cell-culture studies on neurofibromatosis (von Recklinghausen's disease). III. Experiments on X-ray sensitivity.神经纤维瘤病(冯·雷克林豪森病)的细胞培养研究。III. X射线敏感性实验。
Arch Dermatol Res. 1985;277(6):439-43. doi: 10.1007/BF00510059.
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Carrier detection in xeroderma pigmentosum.着色性干皮病的携带者检测
J Clin Invest. 1990 Jan;85(1):135-8. doi: 10.1172/JCI114403.
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Conditions for inhibiting and enhancing effects of the protease inhibitor antipain on x-ray-induced neoplastic transformation in hamster and mouse cells.蛋白酶抑制剂抗痛素对仓鼠和小鼠细胞中X射线诱导的肿瘤转化的抑制和增强作用的条件。
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