Iron is critical for many aspects of cellular function, but it can also generate reactive oxygen species that can damage biological macromolecules. To limit oxidative stress, iron acquisition and its distribution must be tightly regulated. In the lungs, which are continuously exposed to the atmosphere, the risk of oxidative damage is particularly high because of the high oxygen concentration and the presence of significant amounts of catalytically active iron in atmospheric particulates. An effective system of metal detoxification must exist to minimize the associated generation of oxidative stress in the lungs. Here we summarize the evidence that a number of specific proteins that control iron uptake in the gastrointestinal tract are also employed in the lung to transport iron into epithelial cells and sequester it in a catalytically inactive form in ferritin. Furthermore, these and other proteins facilitate ferritin release from lung cells to the epithelial and bronchial lining fluids for clearance by the mucociliary system or to the reticuloendothelial system for long-term storage of iron. These pathways seem to be the primary mechanism for control of oxidative stress presented by iron in the respiratory tract.
|Idioma original||English (US)|
|Número de páginas||8|
|Publicación||Free Radical Biology and Medicine|
|Estado||Published - abr 1 2004|
ASJC Scopus subject areas
- Physiology (medical)