A study of maternofetal iron transfer in the riboflavin-deficient rat.

During gestation iron is diverted from maternal tissues to satisfy fetal requirements, but the factors controlling this transfer are not well understood. Riboflavin may be important in this process, because it is believed to be involved in the mobilization of iron from tissue ferritin. An experiment was designed to test this possibility. Female Norwegian Hooded rats were fed a riboflavin-deficient diet (B2-) from 10 wk of age through to mating and gestation. Control animals fed a complete diet (B2+) were weight-matched to the rats fed the B2- diet. At d 17 or 20 of gestation 59Fe was administered to the dam, and distribution of 59Fe between maternal, placental and fetal tissues was determined 24 h later. Iron-mobilizing activity in placental mitochondria preparations was reduced in riboflavin-deficient rats at d 18 of gestation. Riboflavin deficiency was associated with a reduction in the percentage of the radioiron dose reaching the fetal tissue at both stages of gestation. Maternal hepatic iron stores and plasma iron levels were greater in B2- dams than in controls at d 18 of gestation and showed a reduced rate of depletion over the subsequent 3 d. However, concentrations of radioiron and of ferritin iron and nonheme iron in the fetal tissues were unaffected by riboflavin status. The primary effect of riboflavin deficiency appeared to be a reduction in fetal mass, which served to limit maternal iron depletion and maternofetal iron transfer.