增强代矿物粉尘引起的吞噬细胞的自由基。

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施Vallyathan V,大型摩根富林明,X,中间人NS

增强代矿物粉尘引起的吞噬细胞的自由基。

和细胞杂志。1992年4月,6 (4):404 - 13。

PubMed ID

1312851 (在PubMed

]

文摘

几项研究已经表明,石棉肺毒性和硅可以通过oxidant-induced介导的细胞损伤。我们最近报道表面自由基与新鲜骨折硅细胞损伤可能是一个重要的因素和肺病的感应。虽然在除尘室含氧自由基的生成交互已经证明,没有数据关联粉尘的毒性的氧自由基生成的灰尘与吞噬细胞在其交互。在目前的研究中,我们调查了体外生成氧自由基从人类中性粒细胞和大鼠肺泡巨噬细胞刺激新鲜骨折二氧化硅,二氧化硅岁铁石棉,青石棉,温石棉,无毒的尘埃,重晶石。电子自旋共振(ESR)自旋的援助陷阱phenyl-N-tert-butyl nitrone (PBN)是用来测量氧自由基生成过程中粉尘的吞噬作用。的相对毒性指数和ESR峰值高度,同等面积的基础上和规范化重晶石,显示的直接关系。规范化毒性指数和峰值的高度是:二氧化硅,3.5和2;温石棉,4比2;青石棉,11和8;和铁石棉,26岁和13所示。 Addition of hydroxyl radical scavengers such as catalase, dimethyl sulfoxide, 1,3 dimethyl-2-thiourea (DMTU), sodium benzoate, and mannitol prevented the radical generation. Carmustine, a glutathione reductase-glutathione peroxidase inhibitor, caused a 5-fold increase in the radical generation. These results indicate that a nontoxic dust such as barite generates toxic oxygen radicals at a minimal level that can be quenched by the normal cellular defense system. For toxic dusts such as silica, amosite, chrysotile, and crocidolite, the potential for oxygen radical generation is enhanced by their surface properties, physical dimensions, and the surface-based radical-generating redox sites. The enhanced radical generation may impair the cellular defense system, resulting in cell injury. Use of scavengers, chelators, and potentiating agents suggests the membrane-based oxidase system as the probable primary source of the radical-generating system. The data presented herein suggest the generation of oxygen free radicals as an important primary event in silica- as well as asbestos-induced cell injury.

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药物	目标	类	生物	药理作用	行动
卡莫司汀	谷胱甘肽还原酶、线粒体	蛋白质	人类	是的	抑制剂	细节