Transportation and hemostasis of iron in the cell

Iron is a metal ion in the body that plays a critical role in various physiological functions, including DNA synthesis, mitochondrial respiration, and oxygen transport. Iron in the food sources is primarily absorbed via endocytosis—mediated by divalent metal transporter1 (DMT1)—in the duodenum and is transported by transferrin in blood. Transferrin binds its receptor (TfR) on the surface of the target cells and enters into the cell by receptor mediated-endocytosis. The acidic medium of the endosome causes to release of iron from transferrin. The resulting iron introduces to the cytoplasm by the DMT1 transporter. Iron can be transported to mitochondria, contribute to the synthesis of heme or sulfur-iron cluster, and may remain in the cytoplasm and be stored by ferritin. Under normal conditions, iron binds ferritin in the redox-inactive Fe3+ state, and a small quantity of redox-active Fe2+ irons is needed to contribute to cellular metabolism. Therefore, all mechanisms involving the transportation and homeostasis of iron must be strongly regulated to prevent excess iron from cytotoxic reactions. The iron response protein (IRP)/iron response element (IRE) system carries more regulation of iron homeostasis in the cell. If IRE is located in 5′-UTR of target genes mRNA, IRP cannot connect to IRE in the presence of iron. Thus, mRNA would be translated, and protein can be synthesized, such as ferritin. However, when IRE is in 3′-UTR of mRNA, in the presence of iron, mRNA would be degraded by nucleases, and thus related proteins cannot be synthesized, such as TfR and DMT. Given the role of iron in physiologic functions, any disruption in the regulation of iron transportation or homeostasis increases or decreases the amount of iron in the cell and can affect physiologic functions. If you are looking for high quality, high purity, and cost-effective Iron oxide, or if you require the latest price, please feel free to email contact mis-asia.