Role of surface complexed iron in oxidant generation and lung inflammation induced by silicates.
Ghio-AJ; Kennedy-TP; Whorton-AR; Crumbliss-AL; Hatch-GE; Hoidal-JR
Am J Physiol, Lung Cell Mol Physiol 1992 Nov; 263(5):L511-L518
The pathogenesis of the pulmonary damage caused by the inhalation of silicates was studied by examining the effects of iron (7439896) complexation on oxidant generation in-vitro and in-vivo. The mineral dusts studied included silica (14808607), crocidolite (12001284), kaolinite (1318747), and talc (14807966). Significant concentrations of surface iron were seen in all of the mineral oxide dusts and all were able to further adsorb more iron in quantities greater than rutile, a control substance, when examine in-vitro. Intratracheal infusion of Sprague-Dawley-rats with 20 milligrams of one of the mineral dusts, followed by the examination of lung tissue 96 hours later, demonstrated that all dusts had adsorbed iron onto their surfaces in greater amounts than rutile. As the concentration of surface complexed iron increased, an increase in thiobarbituric- acid reactive products of deoxyribose was seen. Oxidant generation was increased upon iron loading of the mineral oxide surface. The chemiluminescent response of alveolar macrophages indicative of a respiratory burst and the release of leukotriene-B4 were induced with the addition of wetted silica, crocidolite, kaoline, and talc; these responses were enhanced using iron loaded dusts. A cellular influx and an increase in bronchoalveolar protein was seen in rats following injection of wetted silica. Iron loading the silica further increased these changes. The authors conclude that the pulmonary disease caused by silicate exposure may in part be due to the surface complexation of iron.
NIOSH-Publication; NIOSH-Grant; Pulmonary-system-disorders; Silicon-compounds; Lung-disease; Toxic-effects; Molecular-biology; Pathogenicity; Iron-compounds; Mineral-dusts; Laboratory-animals
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American Journal of Physiology: Lung Cellular and Molecular Physiology
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