| dc.creator | GHIO,ANDREW J | |
| dc.creator | TURI,JENNIFER L | |
| dc.creator | YANG,FUNMEI | |
| dc.creator | GARRICK,LAURA M | |
| dc.creator | GARRICK,MICHAEL D | |
| dc.date | 2006-01-01 | |
| dc.date.accessioned | 2019-05-02T21:21:28Z | |
| dc.date.available | 2019-05-02T21:21:28Z | |
| dc.identifier | https://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100008 | |
| dc.identifier.uri | http://revistaschilenas.uchile.cl/handle/2250/81620 | |
| dc.description | 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. | |
| dc.format | text/html | |
| dc.language | en | |
| dc.publisher | Sociedad de Biología de Chile | |
| dc.relation | 10.4067/S0716-97602006000100008 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.source | Biological Research v.39 n.1 2006 | |
| dc.subject | Lung diseases | |
| dc.subject | oxidative stress | |
| dc.subject | SLC11A2 protein | |
| dc.subject | SLC40A1 protein | |
| dc.title | Iron homeostasis in the lung | |
