Oral administration Non-heme and heme oral<unk> s are absorbed into the systemic circulation via different mechanisms. Non-heme<unk>  is present in a form of Fe3+ and undergoes reduction to Fe2+ in the duodenum by duodenal cytochrome b (Dcyt b). Reduced<unk>  is then imported into divalent metal transporter 1(DMT1) into the enterocyte cytoplasm, either transported into bloodstream by the basolateral transport protein ferroportin or stored as ferritin. For heme<unk> , heme oxygenase catalyzes the release of Fe2+ from heme, and Fe2+ enters the enterocyte cytosolic<unk>  pool. However, the uptake mechanism is not well-understood. Haem carrier protein 1(HCP1) has been suggested to transport heme<unk>  into the enterocyte, but has later been proven to have a much higher affinity in the transportation of folate. The absorption of heme<unk>  is 2–3 times faster than non-heme<unk> . After absorption, the<unk>  from<unk>  becomes part of the<unk>  pool in the body. Upon stimulation, the reduction of<unk>  storage Fe3+ in the enterocyte to Fe2+ ferroportin allows the passage of<unk>  through the cell membrane for export. In the blood, ferroportin is then converted to transferrin to reach other tissues. The gastrointestinal (GI) absorption process depends on many factors, including the dosage form, dose, endogenous erythropoiesis process and diet. The most significant factor regulating<unk>  uptake is the amount of<unk>  present in the body.<unk>  absorption increases with sufficient<unk>  storage and vice versa. Increased erythrocyte synthesis also stimulates<unk>  absorption in the gut. Therefore, oral bioavailability of<unk>  varies greatly, ranging from less than 1% to greater than 50%. Uptake of<unk>  can be enhanced by dietary heme<unk>  and vitamin C, while inhibited by calcium, polyphenols, tannins and phytates. Parenteral administration<unk>  Sucrose Intravenous Drip Intravenous<unk>  is administered directly to the bloodstream, in a form of<unk>  carbohydrate complexes, such as<unk>  dextran and<unk>  sucrose. The complex is composed of a polynuclear Fe3+ hydroxide core with a surrounding carbohydrate shell. In the body, the<unk>  complex behaves like a prodrug, releasing the<unk>  from the Fe3+ hydroxide core via metabolism. After the<unk>  complex reaches the bloodstream, macrophages of the reticuloendothelial system will take up the stable complex by endocytosis. The fusion of endosomes and lysosome provides an acidic and reducing environment for<unk>  complex cleavage. Fe2+ released is then transported by the divalent metal transporter 1(DMT1) to the macrophage cytoplasm and incorporated into ferritin. Ferritin is temporarily stored in the macrophages as part of the<unk>  pool in the body. Upon stimulation,<unk>  can be transported out as ferroportin and oxidized into transferrin in the sites of action, such as the bone marrow for red blood cell synthesis or in the liver as the storage form of ferritin. Role of<unk>  in hemoglobin synthesis Hemoglobin Hemoglobin synthesis comprises globin and heme synthesis. The heme molecule is formed by the attachment of an Fe2+ ion to protoporphyrin in the bone marrow cells. Elimination<unk>  obtained from<unk>  is eliminated from the body in a similar manner as dietary<unk> .<unk>  is mostly conserved and recycled in the body with minimal loss. A very limited loss is estimated to be approximately 1 mg/day, mainly by sweating and epithelial cell exfoliation on the skin, genitourinary tract, and gastrointestinal tract. For women, menstrual bleeding is another route for<unk>  loss.
Iron preparation
Iron supplement
Deferoxamine
Phosphate supplement
Protein supplement
Electrocution
Chelation therapy
Zinc pyrithione