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A Study of Maternofetal Iron Transfer in the Riboflavin-Deficient Rat¹

Medical Research Council, Dunn Nutritional Laboratory, Cambridge CB4 1XJ, United Kingdom

During gestation iron is diverted from maternal tissues to satisfy fetal requirements, but the factors controlling this transfer are not well understood. Ribofiavin 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.

KEY WORDS: • riboflavin • pregnancy • iron • fetuses

¹ This work was supported by a postdoctoral award from F. Hoffmann-La Roche and Co. Ltd., Basel, Switzerland.

Manuscript received 2 May 1986. Revision accepted 8 January 1987.

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