Iron homeostasis in the lung

• ANDREW J GHIO ^[2] ; JENNIFER L TURI ^[3] ; FUNMEI YANG ^[1] ; LAURA M GARRICK ^[4] ; MICHAEL D GARRICK ^[4]
  1. [1] University of Texas Health Science Center

     University of Texas Health Science Center

     Estados Unidos

     
  2. [2] Office of Research and Development, United States Environmental Protection Agency Office of Research and Development National Health and Environmental Effects Research Laboratory
  3. [3] Duke University Medical Center
  4. [4] SUNY Department of Biochemistry

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• Localización: Biological Research, ISSN-e 0717-6287, ISSN 0716-9760, Vol. 39, Nº. 1, 2006, págs. 67-77
• Idioma: inglés
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• Resumen

  • Iron is essential for many aspects of cellular function. However, it also can generate oxygen-based free radicals that result in injury to biological molecules. For this reason, iron acquisition and distribution are tightly regulated. Constant exposure to the atmosphere results in significant exposure of the lungs to catalytically active iron. The lungs have a mechanism for detoxification to prevent associated generation of oxidative stress. Those same proteins that participate in iron uptake in the gut are also employed in the lung to transport iron intracellularly and sequester it in an inactive form within ferritin. The release of metal is expedited (as transferrin and ferritin) from lung tissue to the respiratory lining fluid for clearance by the mucocilliary pathway or to the reticuloendothelial system for long-term storage. This pathway is likely to be the major method for the control of oxidative stress presented to the respiratory tract.