Depletion of Iron and Ascorbate in Rodents Diminishes Lung Injury After Silica

Exposures of the lung to iron chelates can be associated with an injury. The catalysis of oxygen-based free radicals is postulated to participate in this injury. Such oxidant generation by mineral oxide particles can be dependent on availability of both iron and a reductant. We tested the study hypo...

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Bibliographic Details
Published in:Experimental lung research 1998, Vol.24 (2), p.219-232
Main Authors: Ghio, Andrew J., Kennedy, Thomas P., Crissman, Kay M., Richards, Judy H., Hatch, Gary E.
Format: Article
Language:English
Subjects:
Animals
Ascorbic Acid - metabolism
Ascorbic Acid Deficiency - metabolism
Biological and medical sciences
Chemical and industrial products toxicology. Toxic occupational diseases
Diet
Disease Models, Animal
Dust
free radicals
Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.)
Iron - deficiency
Iron - metabolism
Lung - drug effects
Lung - metabolism
Male
Medical sciences
pulmonary disease
Pulmonary Fibrosis - chemically induced
Pulmonary Fibrosis - prevention & control
Rats
Rats, Sprague-Dawley
Silicon Dioxide - toxicity
Silicosis - prevention & control
Toxicology
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Summary:Exposures of the lung to iron chelates can be associated with an injury. The catalysis of oxygen-based free radicals is postulated to participate in this injury. Such oxidant generation by mineral oxide particles can be dependent on availability of both iron and a reductant. We tested the study hypothesis that lung injury after silica is associated with the availability of both iron and ascorbate in the host by depleting this metal and reductant in the lungs of rats and guinea pigs, respectively. Rats were fed either a normal diet or a diet deficient of iron. After 30 days, animals were instilled with either saline or 1.0 mg Minusil-5 silica. Relative to saline, silica significantly increased neutrophils and lavage protein. Iron depletion significantly diminished both the cellular influx and injury but only at 1 week after silica exposure. Guinea pigs were provided either a normal diet supplemented with 1,000 ppm vitamin Cora diet deficient in ascorbate. After 14 days, the guinea pigs were instilled with either saline or 1.0 mg silica. Silica exposure significantly increased neutrophils and lavage protein. Ascorbate depletion significantly diminished the influx of inflammatory cells and injury at both 1 day and 1 week after silica exposure. We conclude that host concentrations of both iron and ascorbate can affect lung injury after silica exposure.
ISSN:0190-2148
1521-0499
DOI:10.3109/01902149809099584