Iron homeostasis in the lung following asbestos exposure.
Human exposure to asbestos can cause a wide variety of pulmonary diseases, including pneumoconiosis (i.e., asbestosis). This lung injury is mediated by oxidant generation which increases with the concentration of iron associated with the asbestos. Iron from host sources is complexed by the surface of these fibrous silicates following introduction into the lower respiratory tract. Using bronchoalveolar lavage from unexposed and exposed workers, we demonstrate that asbestos disrupts the normal iron homeostasis in the lungs. Based on these findings, we propose a model of oxidative stress and human lung injury after asbestos exposure.
Ghio
Andrew J
AJ
Stonehuerner
Jacqueline
J
Richards
Judy
J
Devlin
Robert B
RB
D001194:Asbestos / Q000633:toxicity*; D004781:Environmental Exposure; D005293:Ferritins / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007501:Iron / Q000378:metabolism*; D007781:Lactoferrin / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D008954:Models, Biological; D016877:Oxidants / Q000378:metabolism / Q000633:toxicity; D014168:Transferrin / Q000378:metabolism
D016877:Oxidants; D014168:Transferrin; D001194:Asbestos; D005293:Ferritins; D007501:Iron; D007781:Lactoferrin