Iron Complexation by Silica and Silicate Surfaces Is Associated with Oxidant Generation and Acute Inflammatory Lung Injury in the Rat

摘要

The possibility was examined that silica (14808607) and silicate dust exposure to ferric ion resulted in the surface complexation of iron with subsequent increases in in-vitro oxidant generation, in-vitro leukotriene-B4 release by alveolar macrophages, and acute inflammatory lung injury in the rat. Mineral dusts tested were minusil-5, crocidolite (12001284), kaolinite (1318747), and talc (14807966); titanium-dioxide was used as a control. Once exposed to ferric-chloride (7705080) at 1.0 micromolar to 1.0 millimolar concentrations, silica and silicates complexed more than ten times the iron onto their surfaces as did titanium-dioxide. Similarly, silica demonstrated a greater capacity than did titanium-dioxide to complex iron from body sources after intratracheal injection in rats. Three varieties of silica and silicate dusts were prepared by either iron loading their surfaces, wetting them with water, or treating them with deferoxamine in order to investigate the role of complexed iron in oxidant generation, mediator release, and acute inflammatory lung injury after mineral dust exposure. In-vitro generation of hydroxyl radical in an ascorbate/hydrogen-peroxide system, in-vitro luminol chemiluminescence and leukotriene-B4 release by alveolar macrophages, and acute inflammatory lung injury in the rat all increased with surface complexed iron.