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碱性蔗糖沉降分析作为着色性干皮病成纤维细胞对4-硝基喹啉-1-氧化物损伤修复能力的指标。

Alkaline sucrose sedimentation analysis as an indicator of repair capability of xeroderma pigmentosum fibroblasts for 4-nitroquinoline-1-oxide damage.

作者信息

Walker I G

出版信息

Carcinogenesis. 1981;2(8):691-5. doi: 10.1093/carcin/2.8.691.

DOI:10.1093/carcin/2.8.691
PMID:6793257
Abstract

4-Nitroquinoline-1-oxide (4NQO) damage to DNA and its repair in normal and xeroderma pigmentosum (XP) fibroblast stains were followed by sedimentation in an alkaline sucrose gradient. Two forms of analysis were employed. In the brief lysis technique, the cells were exposed to alkali for 30 min before centrifuging. In the long lysis technique, the cells were exposed to alkali overnight before centrifuging. The fibroblast cultures were derived from 6 normal individuals, 2 XP variants, 2 from complementation group C and 1 each from complementation groups A, B and E. by means of the brief lysis technique all of the fibroblasts were found to repair the 4NQO induced damage. By means of the long lysis technique the fibroblasts from normal individuals, from XP variants and from XP group E were found to repair the 4NQO induced damage. The fibroblasts from groups A, B and C showed no repair of the lesion. This latter result, on the repair capability of 4NQO damaged XP cells, correlates with the repair capability of XP cells shown by other methods. It suggest that if sedimentation analysis in alkaline sucrose is to be used to demonstrate the induction of chemically induced damage to DNA and its repair, both brief and long lysis periods should be employed.

摘要

通过碱性蔗糖梯度沉降法,对4-硝基喹啉-1-氧化物(4NQO)对正常及着色性干皮病(XP)成纤维细胞株DNA的损伤及其修复情况进行了跟踪研究。采用了两种分析形式。在短时间裂解技术中,细胞在离心前先暴露于碱中30分钟。在长时间裂解技术中,细胞在离心前先暴露于碱中过夜。成纤维细胞培养物来源于6名正常个体、2名XP变异型个体、2名C互补组个体以及A、B和E互补组各1名个体。通过短时间裂解技术发现,所有成纤维细胞都能修复4NQO诱导的损伤。通过长时间裂解技术发现,正常个体、XP变异型个体以及XP E组的成纤维细胞能修复4NQO诱导的损伤。A、B和C组的成纤维细胞未显示出损伤修复。4NQO损伤的XP细胞的后一修复能力结果,与其他方法显示的XP细胞修复能力相关。这表明,如果要用碱性蔗糖沉降分析法来证明化学诱导的DNA损伤及其修复,应同时采用短时间和长时间裂解期。

相似文献

1
Alkaline sucrose sedimentation analysis as an indicator of repair capability of xeroderma pigmentosum fibroblasts for 4-nitroquinoline-1-oxide damage.碱性蔗糖沉降分析作为着色性干皮病成纤维细胞对4-硝基喹啉-1-氧化物损伤修复能力的指标。
Carcinogenesis. 1981;2(8):691-5. doi: 10.1093/carcin/2.8.691.
2
Defective repair of a class of 4NQO-induced alkali-labile DNA lesions in xeroderma pigmentosum complementation group A fibroblasts.着色性干皮病A互补组成纤维细胞中一类4NQO诱导的碱不稳定DNA损伤的修复缺陷。
Carcinogenesis. 1985 Apr;6(4):555-9. doi: 10.1093/carcin/6.4.555.
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DNA damage and its repair in human normal or xeroderma pigmentosum fibroblasts treated with 4-nitroquinoline 1-oxide or its 3-methyl derivative.用4-硝基喹啉1-氧化物或其3-甲基衍生物处理的人正常或着色性干皮病成纤维细胞中的DNA损伤及其修复
Carcinogenesis. 1981;2(12):1359-62. doi: 10.1093/carcin/2.12.1359.
5
The response to DNA damage induced by 4-nitroquinoline-1-oxide or its 3-methyl derivative in xeroderma pigmentosum fibroblasts belonging to different complementation groups: evidence for different epistasis groups involved in the repair of large adducts in human DNA.4-硝基喹啉-1-氧化物或其3-甲基衍生物诱导的DNA损伤在属于不同互补组的着色性干皮病成纤维细胞中的反应:参与人类DNA中大型加合物修复的不同上位性组的证据。
Carcinogenesis. 1987 Aug;8(8):1071-5. doi: 10.1093/carcin/8.8.1071.
6
Clustered repair of excisable 4-nitroquinoline-1-oxide adducts in a larger fraction of genomic DNA of xeroderma pigmentosum complementation group C cells.着色性干皮病C互补组细胞基因组DNA中较大比例的可切除4-硝基喹啉-1-氧化物加合物的聚集修复。
Carcinogenesis. 1989 Oct;10(10):1777-85. doi: 10.1093/carcin/10.10.1777.
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Enhanced bioreduction of 4-nitroquinoline 1-oxide by cultured ataxia telangiectasia cells.培养的共济失调毛细血管扩张症细胞对4-硝基喹啉1-氧化物的生物还原作用增强
Carcinogenesis. 1988 Sep;9(9):1711-5. doi: 10.1093/carcin/9.9.1711.
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Repair of 4-nitroquinoline-1-oxide-induced DNA damage in normal human cells and cells from classical and variant xeroderma pigmentosum.4-硝基喹啉-1-氧化物诱导的正常人细胞以及经典型和变异型着色性干皮病患者细胞中的DNA损伤修复
Mutat Res. 1983 Feb;112(1):33-46. doi: 10.1016/0167-8817(83)90022-6.
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Repair of DNA damage after exposure to 4-nitroquinoline-1-oxide in heterokaryons derived from xeroderma pigmentosum cells.着色性干皮病细胞来源的异核体暴露于4-硝基喹啉-1-氧化物后DNA损伤的修复
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DNA excision in repair proficient and deficient human cells treated with a combination of ultraviolet radiation and acridine mustard (ICR-170) or 4-nitroquinoline 1-oxide.用紫外线和吖啶芥末(ICR - 170)或4 - 硝基喹啉 - 1 - 氧化物联合处理的修复能力正常和缺陷的人类细胞中的DNA切除
Chem Biol Interact. 1980 Jan;29(1):31-42. doi: 10.1016/0009-2797(80)90084-8.

引用本文的文献

1
The ultimate carcinogen of 4-nitroquinoline 1-oxide does not react with Z-DNA and hyperreacts with B-Z junctions.4-硝基喹啉1-氧化物的最终致癌物不与Z-DNA反应,而与B-Z连接区发生超反应。
Nucleic Acids Res. 1994 Feb 11;22(3):314-20. doi: 10.1093/nar/22.3.314.
2
Molecular basis of 4-nitroquinoline 1-oxide carcinogenesis.4-硝基喹啉1-氧化物致癌作用的分子基础。
Jpn J Cancer Res. 1989 Aug;80(8):691-7. doi: 10.1111/j.1349-7006.1989.tb01698.x.
3
Sequence effect on incision by (A)BC excinuclease of 4NQO adducts and UV photoproducts.(A)BC核酸外切酶对4NQO加合物和紫外线光产物切口的序列效应。
Nucleic Acids Res. 1991 Jan 25;19(2):365-70. doi: 10.1093/nar/19.2.365.