Heme-Up FA Mechanism of Action

Pharmacology: Pharmacodynamics: Mechanism of Action: Carbonyl Iron is a form of the mineral iron. Iron is important for many functions in the body, especially for the transport of oxygen in the blood. Carbonyl Iron is used as a dietary supplement, and to prevent and to treat iron deficiencies and iron deficiency anemia.
Zinc is essential to numerous physiological processes, including the function of many enzymes in the body. Deficiency may lead to poor night vision, slow healing of wounds, poor sexual development and function in males, poor appetite (perhaps owing to a decrease in the sense of taste and smell), a reduced ability to ward off infections, diarrhea, dermatitis, and, in children, retarded growth.
Folic acid enhances chemical reactions that contribute to the production of red blood cells, the manufacture of DNA needed for cell replication, and the metabolism of amino acids (compounds necessary for the manufacture of proteins).
Pharmacokinetics: Carbonyl Iron requires stomach acid for its absorption. Iron in excess of need is stored principally as ferritin in the reticuloendothelial system of liver, spleen, bone marrow and other organs. Iron is released from ferritin in the form of ferrous (Fe II) iron and enters the plasma where it is oxidized by ceruplasmin to ferric (Fe III) iron and taken up and transported in the plasma by transferrin. The body has a limited capacity to excrete iron. Very little iron is excreted by the kidneys or via the biliary route. Some iron losses occur through sloughing of skin and mucosal cells. 20% to 30% of dietary Zinc is absorbed from the GI tract. The main excretion route is through the intestine. Only minor amounts are lost in urine (-2%).
Folic acid is rapidly absorbed from the gastrointestinal tract, mainly from the duodenum and jejunum. Dietary folates are stated to be less well absorbed than crystalline folic acid. The naturally occurring folate polyglutamates are largely deconjugated and reduced by dihydrofolate reductase in the intestine to form 5-methyltetrahydrofolate, which appears in the portal circulation, where it is extensively bound to plasma proteins. Folic acid administered therapeutically enters the portal circulation largely unchanged. Since it is a poor substrate for reduction by dihydrofolate reductase, it is converted to the metabolically active form 5-methyltetrahydrofolate in the plasma and liver.
The principal storage site of folate is the liver, it is also actively concentrated in the CSF, Folate undergoes enterohepatic circulation. Folate metabolites are eliminated in the urine and folate in excess of body requirements is excreted unchanged in the urine. Folate is distributed into breast milk, Folic acid is removed by haemodialysis.