Intestinal absorption of zinc: competitive interactions with iron, cobalt, and copper in mice with sex-linked anemia (sla).

Duodenal uptake and transfer of 59Fe and 65Zn and absorptive interactions between iron, zinc, cobalt, and copper were studied in sla mice and in genetically normal Swiss albino control mice. Genetically normal mice with a high iron-absorbing capacity, induced by being fed an iron-deficient diet, showed greater uptake and transfer of 65Zn in duodenum but not ileum, compared with mice with a low iron-absorbing capacity. 59Fe transfer from the duodenal mucosa to the body was lower in sla mice compared with controls and bleeding stimulated the capacity to absorb 59Fe less in sla mice relative to normal controls. In contrast, 65Zn transfer in sla was no different from controls and was not stimulated by bleeding in sla or in control mice. Iron or cobalt in a 10-fold molar excess predominantly lowered 65Zn transfer in both sla and controls, but in a study of the effect of zinc on iron transport only the uptake of 59Fe in sla mice was lowered by excess zinc in the perfusate. The effect of added copper on 65Zn transport was paradoxical; in both sla and control mice copper markedly increased 65Zn uptake relative to perfusates containing 65Zn alone, but transfer in normal mice was lowered whereas it was increased in sla animals. The interaction between zinc and iron does not appear to take place at the site of the genetic defect in sla mice. The lesion in iron transport in these mice is likely due to defective binding and transfer sites in the basolateral membrane; these sites are apparently exclusive for iron and not shared by zinc.