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本文引用的文献

1
Aflatoxin B1-induced 8-hydroxydeoxyguanosine formation in rat hepatic DNA.黄曲霉毒素B1诱导大鼠肝脏DNA中8-羟基脱氧鸟苷的形成。
Carcinogenesis. 1995 Feb;16(2):419-22. doi: 10.1093/carcin/16.2.419.
2
Exposure of mammalian cell cultures to benzo[a]pyrene and light results in oxidative DNA damage as measured by 8-hydroxydeoxyguanosine formation.将哺乳动物细胞培养物暴露于苯并[a]芘和光照下，会导致氧化DNA损伤，这可通过8-羟基脱氧鸟苷的形成来衡量。
Carcinogenesis. 1995 Jan;16(1):133-7. doi: 10.1093/carcin/16.1.133.
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Improved genomic/nuclear DNA extraction for 8-hydroxydeoxyguanosine analysis of small amounts of rat liver tissue.改进用于少量大鼠肝脏组织8-羟基脱氧鸟苷分析的基因组/核DNA提取方法。
Cancer Lett. 1995 Nov 6;97(2):233-9. doi: 10.1016/0304-3835(95)03980-b.
4
Nephrotoxicity and its prevention by vitamin E in ferric nitrilotriacetate-promoted lipid peroxidation.三乙撑四胺铁促进脂质过氧化作用中维生素E对肾毒性的影响及其预防
Biochim Biophys Acta. 1987 Oct 31;922(1):28-33. doi: 10.1016/0005-2760(87)90241-4.
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Nephrotoxicity and renal cell carcinoma after use of iron- and aluminum-nitrilotriacetate complexes in rats.
J Natl Cancer Inst. 1986 Jan;76(1):107-13.
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Formation of 8-hydroxydeoxyguanosine in liver DNA of rats following long-term exposure to a peroxisome proliferator.
Cancer Res. 1989 May 15;49(10):2603-5.
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Formation of 8-hydroxydeoxyguanosine (8-OH-dG) in rat kidney DNA after intraperitoneal administration of ferric nitrilotriacetate (Fe-NTA).腹腔注射次氮基三乙酸铁（Fe-NTA）后大鼠肾脏DNA中8-羟基脱氧鸟苷（8-OH-dG）的形成。
Carcinogenesis. 1990 Feb;11(2):345-7. doi: 10.1093/carcin/11.2.345.
8
An endonuclease activity of Escherichia coli that specifically removes 8-hydroxyguanine residues from DNA.一种来自大肠杆菌的核酸内切酶活性，它能特异性地从DNA中去除8-羟基鸟嘌呤残基。
Mutat Res. 1991 Jan;254(1):1-12. doi: 10.1016/0921-8777(91)90035-n.
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8-Hydroxyguanine, an abundant form of oxidative DNA damage, causes G----T and A----C substitutions.8-羟基鸟嘌呤是氧化性DNA损伤的一种常见形式，可导致G----T和A----C替换。
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10
Ubiquitous presence in mammalian cells of enzymatic activity specifically cleaving 8-hydroxyguanine-containing DNA.在哺乳动物细胞中普遍存在特异性切割含8-羟基鸟嘌呤DNA的酶活性。
Jpn J Cancer Res. 1992 Apr;83(4):351-7. doi: 10.1111/j.1349-7006.1992.tb00114.x.

给予肾致癌物次氮基三乙酸铁后大鼠肾脏中8-羟基鸟嘌呤修复活性的增加。

Increase in the 8-hydroxyguanine repair activity in the rat kidney after the administration of a renal carcinogen, ferric nitrilotriacetate.

作者信息

Yamaguchi R, Hirano T, Asami S, Sugita A, Kasai H

机构信息

Department of Environmental Oncology, University of Occupational and Environmental Health, Kitakyushu, Japan.

出版信息

Environ Health Perspect. 1996 May;104 Suppl 3(Suppl 3):651-3. doi: 10.1289/ehp.96104s3651.

DOI:10.1289/ehp.96104s3651
PMID:8781399
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1469657/
Abstract

One type of oxidative DNA damage, 8-hydroxyguanine (8-OH-Gua), is known to increase in rat kidney DNA after the administration of a renal carcinogen, ferric nitrilotriacetate (Fe-NTA). To determine the involvement of oxygen radicals in Fe-NTA carcinogenesis, we examined whether the 8-OH-Gua repair enzymes are induced in the rat kidney after Fe-NTA administration, in addition to our analysis of the 8-OH-Gua levels in the DNA, because the 8-OH-Gua repair activity is known to be induced in mammalian cells by oxidative stress due to ionizing radiation. The 8-OH-Gua repair enzyme activity was determined with an endonuclease assay using a 22-mer double strand DNA, which contains 8-OH-Gua at a specific position. A significant increase in the 8-OH-Gua repair activity was observed in the rat kidney after a single intraperitoneal injection of Fe-NTA (p < 0.01). This is the first report on the induction of the repair activity for 8-OH-Gua after treatment with a chemical carcinogen. This assay will be useful for evaluating the carcinogenicity of oxygen radical-forming chemicals.

摘要

一种氧化性DNA损伤，即8-羟基鸟嘌呤（8-OH-Gua），已知在给予肾致癌物次氮基三乙酸铁（Fe-NTA）后，大鼠肾脏DNA中的8-羟基鸟嘌呤会增加。为了确定氧自由基在Fe-NTA致癌过程中的作用，除了分析DNA中的8-OH-Gua水平外，我们还研究了给予Fe-NTA后大鼠肾脏中8-OH-Gua修复酶是否被诱导，因为已知电离辐射引起的氧化应激会在哺乳动物细胞中诱导8-OH-Gua修复活性。使用一种在特定位置含有8-OH-Gua的22聚体双链DNA通过核酸内切酶测定法来确定8-OH-Gua修复酶活性。单次腹腔注射Fe-NTA后，大鼠肾脏中观察到8-OH-Gua修复活性显著增加（p < 0.01）。这是关于化学致癌物处理后8-OH-Gua修复活性诱导的首次报道。该测定法将有助于评估形成氧自由基的化学物质的致癌性。