Iron is present in all cells of the body and plays a key role in many biochemical reactions.
There is no evidence that humans are ingesting sufficient zinc to induce anemia. On the other hand, excessive iron supplementation is often a practice among humans and this excessive intake of nonheme iron may have detrimental effect on zinc nutrition.
It is believe that the basis of interaction between these two minerals is their competition for some portion of a common absorptive pathway.
As a general rule, excessive concentration of one divalent ion in the gastrointestinal tract may inhibit absorption of other divalent ions. Conversely, a deficiency of one divalent ion may enhance the absorption of others.
Absorption of iron is hindered by fiber and phosphate and prompted by ascorbic acid, copper and meat proteins.
Copper and iron may interact in numerous ways. At the metabolic level, an interrelationship appears to exist between iron and copper because the role of copper containing ceruplasmin as feroxidase.
Anemia, often accompanied by accumulation of iron in the liver, has been reported on all species studied, including human. Excessive iron in the form of inorganic iron salts decreased copper status and in time resulted in clinical signs of copper deficiency in several animal species.
Also ascorbic acid and iron are interrelated on that activation of several deoxygenases by ferrous iron appears dependent on the presence of ascorbate.
Absorption of iron is controlled strictly, and excretion of iron is limited. Protein is one of the major participants in the tight regulation of iron: bioavailability of dietary iron is influenced by concomitantly ingested proteins; dietary patterns and protein status affect iron status; additionally, specialized proteins are instrumental in iron absorption and transport.
Interaction of Iron with Other Nutrient
