Iron is an indispensable mineral that the human body relies on for numerous physiological processes. Among its various chemical states, ferric iron represents a specific form where the iron atom carries a particular electrical charge.
The Two Forms of Iron
Iron primarily exists in two distinct chemical states: ferric and ferrous. Their difference lies in their oxidation state. Ferrous iron, denoted as Fe²⁺, has lost two electrons, resulting in a positive two charge. Conversely, ferric iron, symbolized as Fe³⁺, has lost three electrons, giving it a positive three charge.
This difference in electron configuration imparts distinct chemical properties to each form. Ferrous iron tends to be more soluble in water across various pH levels, appearing clear when dissolved. In contrast, ferric iron exhibits lower solubility, particularly at pH levels above approximately 3.5, where it can precipitate as an orange or yellow compound.
Ferric Iron in the Human Body
Once consumed, ferric iron undergoes a series of transformations to become usable by the body. The human digestive system cannot directly absorb ferric iron from the diet, as it is largely insoluble at the physiological pH of the small intestine. For absorption to occur, ferric iron must first be converted into its more soluble ferrous (Fe²⁺) state. This conversion primarily takes place in the acidic environment of the stomach and the initial part of the small intestine.
On the brush border of enterocytes, which are the absorptive cells lining the small intestine, an enzyme called duodenal cytochrome B (Dcytb) acts as a ferric reductase. This enzyme facilitates the reduction of insoluble ferric (Fe³⁺) ions to the absorbable ferrous (Fe²⁺) ions. After this reduction, a protein known as divalent metal transporter 1 (DMT1) then transports the ferrous iron across the cell membrane and into the enterocyte.
Once inside the enterocyte, some ferrous iron can be stored, while the rest is prepared for transport into the bloodstream. Before entering circulation, ferrous iron is re-oxidized back to the ferric (Fe³⁺) state. This re-oxidation is catalyzed by copper-containing enzymes such as hephaestin, found on the basolateral membrane of enterocytes, and ceruloplasmin in the plasma. The re-oxidized ferric iron then binds to transferrin, its primary carrier protein in the plasma, allowing it to be transported throughout the body to various tissues that require iron.
Dietary Sources and Absorption
Dietary ferric iron is found primarily as non-heme iron in plant-based foods and fortified products. Common sources include dark leafy greens like spinach, legumes such as lentils and beans, nuts, seeds, and iron-fortified cereals. Unlike heme iron, which is found in animal products and is absorbed more readily, non-heme iron absorption is more sensitive to other dietary components.
Certain substances can significantly influence the body’s ability to convert and absorb non-heme ferric iron. Vitamin C is a notable enhancer of non-heme iron absorption. It aids by forming soluble complexes with ferric iron in the stomach’s acidic environment, preventing its precipitation and maintaining its solubility as it moves into the duodenum. This allows for more efficient reduction and uptake.
Conversely, some compounds can hinder the absorption of non-heme iron. Phytates, present in whole grains, legumes, and nuts, can bind to iron and form insoluble complexes, thereby reducing its bioavailability. Tannins, commonly found in tea and coffee, also inhibit non-heme iron absorption. Calcium, found in dairy products, is another dietary component that can interfere with the absorption of both heme and non-heme iron.