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支持活性氧物种在石棉诱导的毒性和肺部疾病中发挥作用的证据。

Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease.

作者信息

Mossman B T, Marsh J P

机构信息

Department of Pathology, University of Vermont, Burlington 05405.

出版信息

Environ Health Perspect. 1989 May;81:91-4. doi: 10.1289/ehp.898191.

DOI:10.1289/ehp.898191
PMID:2667992
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1567557/
Abstract

Asbestos is an important occupational and environmental toxicant that affects several cell types in the respiratory tract. In an effort to understand how asbestos causes cell injury and/or altered proliferation and differentiation of cells, this laboratory has focused on reactive oxygen species as mediators of asbestos-induced biological effects. A compendium of experimental results reported by this laboratory and others supports this hypothesis. For example, scavengers of reactive oxygen metabolites and iron chelators (i.e., desferroxamine) prevent cytotoxicity after addition of asbestos to a variety of cell lines and macrophages in vitro. DNA strand breakage associated with toxicity of crocidolite asbestos in C3H10T 1/2 cells also is ameliorated with use of desferroxamine. All types of asbestos cause lipid peroxidation in mammalian cells and artificial membranes, a phenomenon that can be prevented by removal of catalytic iron. Last, asbestos causes generation of active oxygen species after interaction with leukocytes or by reduction of oxygen on the surface of the fibers.

摘要

石棉是一种重要的职业和环境毒物,会影响呼吸道中的多种细胞类型。为了了解石棉如何导致细胞损伤和/或细胞增殖及分化改变,本实验室将重点放在活性氧作为石棉诱导生物学效应的介质上。本实验室及其他机构报告的一系列实验结果支持这一假说。例如,活性氧代谢产物清除剂和铁螯合剂(即去铁胺)可在体外将石棉添加到多种细胞系和巨噬细胞后预防细胞毒性。使用去铁胺也可改善与青石棉在C3H10T 1/2细胞中的毒性相关的DNA链断裂。所有类型的石棉都会在哺乳动物细胞和人工膜中引起脂质过氧化,这一现象可通过去除催化铁来预防。最后,石棉在与白细胞相互作用后或通过纤维表面的氧还原作用导致活性氧的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/465e/1567557/04d575c4c755/envhper00425-0090-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/465e/1567557/04d575c4c755/envhper00425-0090-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/465e/1567557/04d575c4c755/envhper00425-0090-a.jpg

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本文引用的文献

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The pathogenesis of asbestos-associated diseases.石棉相关疾病的发病机制。
N Engl J Med. 1982 Jun 17;306(24):1446-55. doi: 10.1056/NEJM198206173062403.
2
Asbestos: mechanisms of toxicity and carcinogenicity in the respiratory tract.石棉:呼吸道中毒性和致癌性机制
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Biopersistence and potential adverse health impacts of fibrous nanomaterials: what have we learned from asbestos?纤维状纳米材料的生物持久性和潜在的健康影响:我们从石棉中学到了什么?
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The role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis.炎症在特发性肺纤维化发病机制中的作用。
Antioxid Redox Signal. 2008 Feb;10(2):287-301. doi: 10.1089/ars.2007.1897.
10
In vivo bioassays of acute asbestosis and its correlation with ESR spectroscopy and imaging in redox status.急性石棉沉着病的体内生物测定及其与氧化还原状态下的电子自旋共振光谱和成像的相关性。
Mol Cell Biochem. 2002 May-Jun;234-235(1-2):369-77.
Br J Exp Pathol. 1984 Feb;65(1):81-90.
4
Asbestos catalyzes hydroxyl and superoxide radical generation from hydrogen peroxide.石棉可催化过氧化氢生成羟基自由基和超氧阴离子自由基。
Arch Biochem Biophys. 1984 Jan;228(1):373-6. doi: 10.1016/0003-9861(84)90078-x.
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Lipid peroxidation in microsomes induced by crocidolite fibres.青石棉纤维诱导微粒体中的脂质过氧化作用。
Chem Biol Interact. 1983 Apr-May;44(1-2):111-8. doi: 10.1016/0009-2797(83)90133-3.
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Asbestos-induced alteration of human peripheral blood monocyte activity.
Int Arch Allergy Appl Immunol. 1982;69(4):302-5. doi: 10.1159/000233190.
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In vitro effect of asbestos fibers on polymorphonuclear leukocyte function.
Int Arch Allergy Appl Immunol. 1982;68(1):17-21. doi: 10.1159/000233061.
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Asbestos-induced decomposition of hydrogen peroxide.石棉诱导的过氧化氢分解。
Environ Res. 1985 Aug;37(2):287-92. doi: 10.1016/0013-9351(85)90108-2.
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Asbestos-catalysed lipid peroxidation and its inhibition by desferroxamine.石棉催化的脂质过氧化及其被去铁胺抑制的情况。
Biochem J. 1985 Jan 1;225(1):259-62. doi: 10.1042/bj2250259.
10
Alteration of superoxide dismutase activity in tracheal epithelial cells by asbestos and inhibition of cytotoxicity by antioxidants.石棉对气管上皮细胞中超氧化物歧化酶活性的影响及抗氧化剂对细胞毒性的抑制作用。
Lab Invest. 1986 Feb;54(2):204-12.