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本文引用的文献

1
THE BIOCHEMISTRY OF DESFERRIOXAMINE AND ITS RELATION TO IRON METABOLISM.去铁胺的生物化学及其与铁代谢的关系。
Ann N Y Acad Sci. 1964 Oct 7;119:758-68. doi: 10.1111/j.1749-6632.1965.tb54077.x.
2
Use of physico-chemical and cell-free assays to evaluate the potential carcinogenicity of fibres.
IARC Sci Publ. 1996(140):35-54.
3
Detection of surface free radical activity of respirable industrial fibres using supercoiled phi X174 RF1 plasmid DNA.使用超螺旋 phi X174 RF1 质粒 DNA 检测可吸入工业纤维的表面自由基活性
Carcinogenesis. 1995 Dec;16(12):2973-9. doi: 10.1093/carcin/16.12.2973.
4
Free radical generation at the solid/liquid interface in iron containing minerals.含铁矿物中固/液界面处的自由基生成。
Free Radic Res. 1995 Dec;23(6):593-614. doi: 10.3109/10715769509065280.
5
Activation of UICC crocidolite: the effect of conversion of some ferric ions to ferrous ions.国际抗癌联盟(UICC)青石棉的活化:部分铁离子转化为亚铁离子的影响。
Environ Res. 1993 Feb;60(2):193-206. doi: 10.1006/enrs.1993.1027.
6
DNA strand breaks following in vitro exposure to asbestos increase with surface-complexed [Fe3+].体外暴露于石棉后,DNA链断裂随表面络合的[Fe3+]增加而增加。
Arch Biochem Biophys. 1994 May 15;311(1):13-8. doi: 10.1006/abbi.1994.1202.
7
Hydroxyl radicals are formed in the rat lung after asbestos instillation in vivo.在体内给大鼠滴注石棉后,大鼠肺内会形成羟基自由基。
Am J Respir Cell Mol Biol. 1994 May;10(5):573-9. doi: 10.1165/ajrcmb.10.5.8179922.
8
Iron associated with asbestos bodies is responsible for the formation of single strand breaks in phi X174 RFI DNA.与石棉小体相关的铁会导致φX174 RFI DNA形成单链断裂。
Occup Environ Med. 1994 Mar;51(3):200-4. doi: 10.1136/oem.51.3.200.
9
Iron-dependent formation of 8-hydroxydeoxyguanosine in isolated DNA and mutagenicity in Salmonella typhimurium TA102 induced by crocidolite.由青石棉诱导的离体DNA中8-羟基脱氧鸟苷的铁依赖性形成及鼠伤寒沙门氏菌TA102中的致突变性。
Carcinogenesis. 1994 Aug;15(8):1749-51. doi: 10.1093/carcin/15.8.1749.
10
Asbestos causes DNA strand breaks in cultured pulmonary epithelial cells: role of iron-catalyzed free radicals.石棉导致培养的肺上皮细胞中的DNA链断裂:铁催化自由基的作用。
Am J Physiol. 1995 Mar;268(3 Pt 1):L471-80. doi: 10.1152/ajplung.1995.268.3.L471.

铁螯合剂处理的闪石石棉的化学表征及反应活性

Chemical characterization and reactivity of iron chelator-treated amphibole asbestos.

作者信息

Gold J, Amandusson H, Krozer A, Kasemo B, Ericsson T, Zanetti G, Fubini B

机构信息

Department of Applied Physics, Chalmers University of Technology, Goteborg, Sweden.

出版信息

Environ Health Perspect. 1997 Sep;105 Suppl 5(Suppl 5):1021-30. doi: 10.1289/ehp.97105s51021.

DOI:10.1289/ehp.97105s51021
PMID:9400694
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1470174/
Abstract

Iron in amphibole asbestos is implicated in the pathogenicity of inhaled fibers. Evidence includes the observation that iron chelators can suppress fiber-induced tissue damage. This is believed to occur via the diminished production of fiber-associated reactive oxygen species. The purpose of this study was to explore possible mechanisms for the reduction of fiber toxicity by iron chelator treatments. We studied changes in the amount and the oxidation states of bulk and surface iron in crocidolite and amosite asbestos that were treated with iron-chelating desferrioxamine, ferrozine, sodium ascorbate, and phosphate buffer solutions. The results have been compared with the ability of the fibers to produce free radicals and decompose hydrogen peroxide in a cell-free system in vitro. We found that chelators can affect the amount of iron at the surface of the asbestos fibers and its valence, and that they can modify the chemical reactivity of these surfaces. However, we found no obvious or direct correlations between fiber reactivity and the amount of iron removed, the amount of iron at the fiber surface, or the oxidation state of surface iron. Our results suggest that surface Fe3+ ions may play a role in fiber-related carboxylate radical formation, and that desferrioxamine and phosphate groups detected at treated fiber surfaces may play a role in diminishing and enhancing, respectively, fiber redox activity. It is proposed that iron mobility in the silicate structure may play a larger role in the chemical reactivity of asbestos than previously assumed.

摘要

角闪石石棉中的铁与吸入纤维的致病性有关。证据包括观察到铁螯合剂可以抑制纤维诱导的组织损伤。据信这是通过减少纤维相关活性氧的产生而发生的。本研究的目的是探索铁螯合剂处理降低纤维毒性的可能机制。我们研究了用铁螯合剂去铁胺、亚铁嗪、抗坏血酸钠和磷酸盐缓冲溶液处理的青石棉和铁石棉中整体和表面铁的含量及氧化态的变化。将结果与纤维在体外无细胞系统中产生自由基和分解过氧化氢的能力进行了比较。我们发现螯合剂可以影响石棉纤维表面的铁含量及其化合价,并且可以改变这些表面的化学反应性。然而,我们没有发现纤维反应性与去除的铁量、纤维表面的铁量或表面铁的氧化态之间存在明显或直接的相关性。我们的结果表明,表面Fe3+离子可能在与纤维相关的羧酸盐自由基形成中起作用,并且在处理过的纤维表面检测到的去铁胺和磷酸基团可能分别在降低和增强纤维氧化还原活性中起作用。有人提出,硅酸盐结构中铁的迁移率在石棉的化学反应性中可能比以前认为的起更大的作用。