Summary. Iron distribution and metabolism have been studied in hereditary iiiicrocytic anaemia of tlie mouse (gene symbol mk), an autosonial recessive trait cliaractcrizcd by hypoclironiia and microcytosis. Evidence of iron deficiency was hutid in the forin of depleted body stores, hyposidcraemia, an increased total iron biiiding capacity of tlic plasma and a high free erythrocyte‐protoporyhyrin level. I lowcvcr, the failure to find citlicr rapid clearance and high utilization of tracer doses of 59Fe or a complete response to pareliteral iron treatment indicated that simple iron deficiency was not the cause of tlie anaemia. It is suggested that generalized impairmcn t in tlie cellular uptake of iron involvingthe transfer of iron from the intestinal lumen to tlic mucosa and from tlie plasma to the erythroblast may provide a unitary explaiiation of licreditary microcytic anaemia.
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Bannerman et al. (1972) studied this question.
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