On the kinetics of iron absorption in mice.

In individuals with similar body stores of iron, the amount of iron absorbed from a single oral dose is not proportional to the amount of iron administered. Although a greater amount of iron is absorbed as the size of the oral dose increases, the percentage or fraction of the dose that is absorbed actually decreases (1-3). In addition, the amount of iron absorbed from a given dose is dependent upon, among other things, the iron stores of the body (1, 4-6). Thus, an individual with deficient iron stores, due solely to deficient iron intake, tends to absorb more iron from a given dose than someone with normal iron stores, while the normal person tends to absorb more iron from the same dose than the individual with excessive iron stores accumulated through a large iron intake. Although it has been established that the size of the dose and the state of the iron stores of the body both influence the absorption of iron, the biological processes through which the absorption of iron is regulated are unknown. It has been suggested that iron absorption may be controlled either by: 1) the degree of saturation of an intracellular iron carrier, e.g., ferritin (7) ; 2) the degree of saturation of a plasma carrier of iron, or transferrin (8); 3) cellular enzymatic mechanisms (9, 10); 4) the tension of oxygen at the cellular level (11); or 5) the degree of erythropoiesis (1). None of these hypotheses has gained wide acceptance. It has recently been observed that the absorption of copper is related to the amount of copper ingested in a manner qualitatively similar to the relationship between dose and amount absorbed for iron (12). An analysis of this relation indicated that copper absorption is mediated through