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Role of surface complexed iron in oxidant generation and lung inflammation induced by silicates.

Authors
Ghio-AJ; Kennedy-TP; Whorton-AR; Crumbliss-AL; Hatch-GE; Hoidal-JR
Source
Am J Physiol, Lung Cell Mol Physiol 1992 Nov; 263(5):L511-L518
NIOSHTIC No.
00211599
Abstract
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.
Keywords
NIOSH-Publication; NIOSH-Grant; Pulmonary-system-disorders; Silicon-compounds; Lung-disease; Toxic-effects; Molecular-biology; Pathogenicity; Iron-compounds; Mineral-dusts; Laboratory-animals
Contact
Medicine University of Tennessee Room H-314, Coleman Bldg Memphis, TN 38163
CODEN
APLPE7
CAS No.
7439-89-6; 14808-60-7; 12001-28-4; 1318-74-7; 14807-96-6
Publication Date
19921101
Document Type
Journal Article
Funding Amount
574424
Funding Type
Grant
Fiscal Year
1993
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-02264
Issue of Publication
5
ISSN
1040-0605
Priority Area
Pulmonary-system-disorders
Source Name
American Journal of Physiology: Lung Cellular and Molecular Physiology
State
TN
Performing Organization
University of Tenn Center Health Scien, Memphis, Tennessee
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