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本文引用的文献

1
Epigenetics and cancer.表观遗传学与癌症。
J Appl Physiol (1985). 2010 Aug;109(2):598-605. doi: 10.1152/japplphysiol.00066.2010. Epub 2010 Mar 4.
2
Mechanisms of c-myc degradation by nickel compounds and hypoxia.镍化合物和缺氧诱导 c-myc 降解的机制。
PLoS One. 2009 Dec 31;4(12):e8531. doi: 10.1371/journal.pone.0008531.
3
Nickel ions inhibit histone demethylase JMJD1A and DNA repair enzyme ABH2 by replacing the ferrous iron in the catalytic centers.镍离子通过取代催化中心的亚铁离子来抑制组蛋白去甲基酶 JMJD1A 和 DNA 修复酶 ABH2。
J Biol Chem. 2010 Mar 5;285(10):7374-83. doi: 10.1074/jbc.M109.058503. Epub 2009 Dec 30.
4
The role of Myc-induced protein synthesis in cancer.Myc诱导的蛋白质合成在癌症中的作用。
Cancer Res. 2009 Dec 1;69(23):8839-43. doi: 10.1158/0008-5472.CAN-09-1970. Epub 2009 Nov 24.
5
Nickel-induced facial dermatitis: adolescents beware of the cell phone.镍诱发的面部皮炎:青少年谨防手机。
Cutis. 2009 Oct;84(4):199-200.
6
Nickel induces intracellular calcium mobilization and pathophysiological responses in human cultured airway epithelial cells.镍诱导人呼吸道上皮细胞内钙动员和病理生理反应。
Chem Biol Interact. 2010 Jan 5;183(1):25-33. doi: 10.1016/j.cbi.2009.09.011.
7
Heavy metal hazards of pediatric syrup administration in Nigeria: a look at chromium, nickel and manganese.尼日利亚小儿糖浆剂服用中的重金属危害:铬、镍和锰的研究
Int J Environ Res Public Health. 2009 Jul;6(7):1972-9. doi: 10.3390/ijerph6071972. Epub 2009 Jul 9.
8
Nickel release from inexpensive jewelry and hair clasps purchased in an EU country - Are consumers sufficiently protected from nickel exposure?在欧盟国家购买的廉价珠宝和发夹的镍释放情况——消费者是否得到了足够的保护以避免镍暴露?
Sci Total Environ. 2009 Oct 1;407(20):5315-8. doi: 10.1016/j.scitotenv.2009.06.034. Epub 2009 Jul 24.
9
Heterochromatinization as a potential mechanism of nickel-induced carcinogenesis.异染色质化作为镍诱导致癌作用的一种潜在机制。
Biochemistry. 2009 Jun 2;48(21):4626-32. doi: 10.1021/bi900246h.
10
Children's clothing fasteners as a potential source of exposure to releasable nickel ions.儿童服装扣件作为可释放镍离子的潜在暴露源。
Contact Dermatitis. 2009 Feb;60(2):100-5. doi: 10.1111/j.1600-0536.2008.01487.x.

探讨镍诱导遗传毒性和致癌性的分子机制:文献综述。

Exploring the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity: a literature review.

机构信息

Environmental Toxicology Research Laboratory, NIH RCMI-Center for Environmental Health, Jackson State University, Jackson, MS 39217, USA.

出版信息

Rev Environ Health. 2011;26(2):81-92. doi: 10.1515/reveh.2011.012.

DOI:10.1515/reveh.2011.012
PMID:21905451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3172618/
Abstract

Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil- and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel can also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart, and testes can also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.

摘要

镍是一种天然存在的元素,以多种矿物形式存在,主要存在于土壤和沉积物中,其迁移受土壤物理化学性质的影响。镍的工业来源包括电镀、合金生产、不锈钢和镍镉电池等冶金过程。镍工业、石油和燃煤电厂以及垃圾焚烧炉都被认为是将镍释放到环境中的原因。在人类中,镍毒性受暴露途径、剂量和镍化合物的溶解度的影响。肺部吸入是镍诱导毒性的主要暴露途径。镍也可以通过皮肤摄入或吸收。主要靶器官是肾脏和肺部。其他器官,如肝脏、脾脏、心脏和睾丸,也可能受到较小程度的影响。尽管最常见的健康影响是过敏反应,但研究还表明镍对人类具有致癌性。本综述的重点是最近关于镍诱导遗传毒性和致癌性的分子机制的研究。我们首先介绍了镍在环境中的存在、人类暴露和人类健康影响的背景。