The effect of acute changes in erythron demands and in plasma-
iron turnover (PIT) on the in vitro and in vivo absorption of 59Fe3+ was studied in the mouse. Hypoxic exposure for 20 h (a time at which intestinal
iron absorption is markedly stimulated) induced
reticulocytosis with a marked elevation in PIT. More prolonged exposure (3 d) further enhanced the plasma-
iron clearance, even though the absorption of 59Fe was not further increased. Recipient mice, exchange transfused with whole blood from
phenylhydrazine-treated animals, had a marked
reticulocytosis and elevated PIT. However, in vivo studies exhibited only a small enhancement in intestinal 59Fe absorption. In vitro studies, in contrast, showed no changes in the kinetic parameters for duodenal Fe3+ uptake in similarly-transfused mice. Blood cells, rather than plasma, were responsible for the enhanced in vivo absorption in the transfused animals. These data indicate that acute changes in body
iron demands and in PIT have only a small effect on
iron absorption via a process independent of the adaptive increase in carrier-mediated uptake following chronic (3 d)
hypoxia. This regulatory process, however, is inadequate to explain the adaptive changes seen during acute (20 h) hypoxic exposure.