Ferrous Iron Oxidation by Intestinal Mucosa: Possible Role in Mucosal Iron Metabolism 1

Abstract

A two–step mechanism for iron absorption has been described in man as well as in experimental animals (1–6). The first, relatively rapid, step is uptake of luminal iron by the mucosal cell. Subsequent transfer out of the cell into the circulation or underlying tissues is slower and only partially complete, thereby providing an intestinal mechanism for the regulation of iron absorption. Unab–sorbed iron is postulated to remain sequestered in the mucosal cell until it is lost in the feces when the cell is desquamated (4, 5).

An earlier study (7) with rat duodenal gut sacs demonstrated that the iron in the mucosa reacted as two chemically distinct forms, Fe²+ and Fe³+. In addition, the Fe²+ fraction was the precursor of the Fe³+ fraction, and the properties of the latter were consistent with the aforementioned sequestered portion of mucosal cell iron. Variable, small portions of the trivalent iron have been identified as ferritin (5, 7, 8), but the major fraction of this pool remains unidentified.

These findings suggested the presence of an intracellular mechanism for the oxidation of Fe²+ to Fe³+, and the present report describes the discovery of such a ferrous–oxidizing activity in the intestine. The physical and chemical properties of this activity are consistent with those of an enzyme and suggest a possible role in mucosal cell iron metabolism for this activity.

Methods. Analytical methods. Total iron was determined by the α,α'–dipyridyl method of Ramsay (9), modified as previously described (3). Aliquots of unknown were mixed with 0.5 ml of 0.5% α,α'–dipyridyl in 1.0 M sodium acetate buffer (pH 4.0) and 0.25 ml of 0.2 M sodium sulfite, diluted to a total volume of 3.25 ml, heated 10 min at 100°, then centrifuged in a clinical centrifuge till clear.