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环境病理学,毒理学和肿瘤学期刊
影响因子: 1.241 5年影响因子: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN 打印: 0731-8898
ISSN 在线: 2162-6537

环境病理学,毒理学和肿瘤学期刊

DOI: 10.1615/JEnvironPatholToxicolOncol.v28.i2.70
pages 153-162

Iron Accumulation and Expression of Iron-Related Proteins Following Murine Exposure to Crocidolite

Andrew J. Ghio
National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, North Carolina; and Department of Pathology, Duke University Medical Center, Durham, North Carolina
Roderick J. Tan
Department of Pathology, University of Pittsburgh, PA 15261
Kathleen Ghio
National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, NC 27711
Cheryl L. Fattman
Department of Environmental and Occupation Health, University of Pittsburgh, PA 15261
Tim D. Oury
Department of Pathology, University of Pittsburgh, PA 15261

ABSTRACT

We tested the postulate that asbestos exposure alters iron homeostasis in the mouse lung. Crocidolite asbestos (100 μg intratracheally) was instilled into C57BL/6 mice. TiO2 served as a control exposure. Using iron staining and immunohistochemistry, concentrations of this metal and expression of several iron transport and storage proteins were evaluated at one day and one month following asbestos exposure. Iron was not stainable one day following asbestos instillation but was increased one month later. There was an elevated expression of duodenal cytochrome b (Dcytb), divalent metal transporter 1 (DMT1), and ferritin at both one day and one month after crocidolite exposure. While ferroportin (FPN1) expression was increased one day after asbestos exposure, levels of this metal exporter had returned to baseline at one month. TiO2 did not affect changes in either the iron concentration or the expression of these iron-related proteins at one day and one month. We conclude that asbestos exposure alters lung iron homeostasis with an accumulation of the metal resulting. Elevations in available iron affect changes in the expression of Dcytb, DMT1, ferritin, and FPN1, which further modify metal homeostasis in the lung.


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