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平台期人类正常成纤维细胞和着色性干皮病成纤维细胞对紫外线细胞毒性作用的抗性。

Resistance of plateau-phase human normal and xeroderma pigmentosum fibroblasts to the cytotoxic effect of ultraviolet light.

作者信息

Chan G L, Little J B

出版信息

Mutat Res. 1979 Dec;63(2):401-12. doi: 10.1016/0027-5107(79)90072-1.

DOI:10.1016/0027-5107(79)90072-1
PMID:522880
Abstract

Clonogenic survival response to 254-nm ultraviolet light was measured in 2 strains of repair-proficient normal human fibroblasts and 4 strains of xeroderma pigmentosum (XP) fibroblasts belonging to complementation groups A, C, D and variant. In all strains except XPA, cells irradiated in plateau phase and subcultured immediately were much more resistant to the lethal effect of UV than cells irradiated in the exponential phase of growth. Typically, 10-20% of plateau-phase cells were extremely resistant. When the cultures were held in plateau phase for 24 h after irradiation and before subculture, there was a further enhance of survival. By use of a UV-specific endonuclease assay, no difference was found in the number of DNA lesions induced in exponentially growing and plateau cultures by the same dose of UV light. Thus plateau-phase cells appear to be more efficient in their DNA-repair capability than cells in exponential growth. XP group A cells were uniquely found to be deficient in the processes which lead to plateau-phase resistance. Since plateau-phase repair was not lacking in XP groups C, D and variant, it may be related to a DNA-repair process different from that which is responsible for the overall UV sensitivity of these cells.

摘要

在2株修复功能正常的正常人成纤维细胞和4株属于互补组A、C、D及变异型的着色性干皮病(XP)成纤维细胞中,测定了对254纳米紫外线的克隆形成存活反应。在除XPA外的所有菌株中,处于平台期照射并立即传代培养的细胞比处于生长指数期照射的细胞对紫外线的致死效应具有更强的抗性。通常,10%至20%的平台期细胞具有极强的抗性。当培养物在照射后且传代培养前在平台期保持24小时时,存活率进一步提高。通过使用紫外线特异性核酸内切酶测定法,发现相同剂量的紫外线在指数生长期和平板期培养物中诱导的DNA损伤数量没有差异。因此,平台期细胞在DNA修复能力上似乎比指数生长期的细胞更有效。独特的是,发现XP组A细胞在导致平台期抗性的过程中存在缺陷。由于XP组C、D及变异型细胞并不缺乏平台期修复,所以它可能与一种不同于导致这些细胞总体紫外线敏感性的DNA修复过程有关。

相似文献

1
Resistance of plateau-phase human normal and xeroderma pigmentosum fibroblasts to the cytotoxic effect of ultraviolet light.平台期人类正常成纤维细胞和着色性干皮病成纤维细胞对紫外线细胞毒性作用的抗性。
Mutat Res. 1979 Dec;63(2):401-12. doi: 10.1016/0027-5107(79)90072-1.
2
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Repair of UV-endonuclease-susceptible sites in the 7 complementation groups of xeroderma pigmentosum A through G.着色性干皮病A至G型7个互补组中紫外线内切酶敏感位点的修复
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Effects of ultraviolet irradiation on the cell cycle in normal and UV-sensitive cell lines with reference to the nature of the defect in xeroderma pigmentosum variant.紫外线照射对正常细胞系和紫外线敏感细胞系细胞周期的影响,参考着色性干皮病变异型缺陷的性质。
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Ultraviolet light-resistant primary transfectants of xeroderma pigmentosum cells are also DNA repair-proficient.
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DNA damage and repair in normal, xeroderma pigmentosum and XP revertant cells analyzed by gel electrophoresis: excision of cyclobutane dimers from the whole genome is not necessary for cell survival.通过凝胶电泳分析正常细胞、着色性干皮病细胞和着色性干皮病回复突变细胞中的DNA损伤与修复:全基因组中环丁烷二聚体的切除对于细胞存活并非必需。
Carcinogenesis. 1989 Sep;10(9):1691-6. doi: 10.1093/carcin/10.9.1691.

引用本文的文献

1
p53-mediated protective responses to UV irradiation.p53介导的对紫外线照射的保护性反应。
Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12255-7. doi: 10.1073/pnas.94.23.12255.
2
The effect of UV irradiation on proliferation and life span of human diploid fibroblast-like cells.紫外线照射对人二倍体成纤维样细胞增殖和寿命的影响。
In Vitro. 1982 Aug;18(8):703-7. doi: 10.1007/BF02796425.
3
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.
4
Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.将原代人成纤维细胞的非分裂群体暴露于紫外线(254纳米)辐射下,可诱导修复潜在致死性细胞损伤的能力出现短暂增强。
Proc Natl Acad Sci U S A. 1984 Feb;81(3):781-4. doi: 10.1073/pnas.81.3.781.
5
The residual repair capacity of xeroderma pigmentosum complementation group C fibroblasts is highly specific for transcriptionally active DNA.着色性干皮病C互补组成纤维细胞的残余修复能力对转录活跃的DNA具有高度特异性。
Nucleic Acids Res. 1990 Feb 11;18(3):443-8. doi: 10.1093/nar/18.3.443.
6
Xeroderma pigmentosum complementation group C cells remove pyrimidine dimers selectively from the transcribed strand of active genes.着色性干皮病C互补组细胞从活性基因的转录链中选择性地去除嘧啶二聚体。
Mol Cell Biol. 1991 Aug;11(8):4128-34. doi: 10.1128/mcb.11.8.4128-4134.1991.