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新鲜破碎的二氧化硅粉尘产生自由基。其在急性二氧化硅诱导的肺损伤中的潜在作用。

Generation of free radicals from freshly fractured silica dust. Potential role in acute silica-induced lung injury.

作者信息

Vallyathan V, Shi X L, Dalal N S, Irr W, Castranova V

机构信息

Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, WV.

出版信息

Am Rev Respir Dis. 1988 Nov;138(5):1213-9. doi: 10.1164/ajrccm/138.5.1213.

Abstract

Data presented here indicate that freshly fractured silica exhibits surface characteristics and biologic reactivity distinct from aged silica, and on this basis we propose that these surface features may lead to enhanced manifestations of lung injury. Grinding of silica produces approximately 10(18) Si and Si-O (silicon-based) radicals per gram of dust on the particulate surface which are characterized by an electron spin resonance (ESR) spectrum centered around g = 2.0015. These silicon-based radicals react with aqueous media to produce OH radicals, which are demonstrable using a DMPO spin trap. The concentration of silicon-based radicals in silica decreases with aging in air and exhibits a half-life of approximately 30 h, whereas its ability to generate OH radicals in aqueous solution decreases with a half-life of approximately 20 h. However, on storage in aqueous media, the concentration of silicon-based radicals and the dust's ability to generate OH radicals decrease significantly within a few minutes. Freshly ground silica is also more biologically reactive than aged silica, because freshly crushed silica activates a greater respiratory burst in alveolar macrophages than aged silica, i.e., storage of ground dust in air decreases silica-induced superoxide anion secretion, hydrogen peroxide release, and NBT reduction by 25%, 68%, and 43%, respectively. Furthermore, compared to aged silica, freshly ground silica exhibits a greater cytotoxic effect on cellular membrane integrity, i.e., a 1.5-fold increase in LDH release from macrophages, a 36-fold increase in hemolytic activity, and a three-fold increase in the ability to induce lipid peroxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

此处呈现的数据表明,新破碎的二氧化硅呈现出与老化二氧化硅不同的表面特征和生物反应性,基于此我们提出,这些表面特征可能导致肺损伤表现增强。研磨二氧化硅会在每克粉尘的颗粒表面产生约10¹⁸个硅和硅氧(硅基)自由基,其电子自旋共振(ESR)光谱以g = 2.0015为中心。这些硅基自由基与水性介质反应生成羟基自由基,可使用DMPO自旋捕集器进行检测。二氧化硅中硅基自由基的浓度会随着在空气中老化而降低,半衰期约为30小时,而其在水溶液中产生羟基自由基的能力半衰期约为20小时。然而,在水性介质中储存时,硅基自由基的浓度及其产生羟基自由基的能力会在几分钟内显著降低。新研磨的二氧化硅比老化的二氧化硅具有更高的生物反应性,因为新破碎的二氧化硅比老化的二氧化硅能在肺泡巨噬细胞中激活更强的呼吸爆发,即研磨后的粉尘在空气中储存会使二氧化硅诱导的超氧阴离子分泌、过氧化氢释放和NBT还原分别降低25%、68%和43%。此外,与老化二氧化硅相比,新研磨的二氧化硅对细胞膜完整性具有更大的细胞毒性作用,即巨噬细胞中乳酸脱氢酶释放增加1.5倍、溶血活性增加36倍以及诱导脂质过氧化的能力增加3倍。(摘要截选至250词)

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