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Pyridoxine Deficiency and Iron Metabolism in the Pregnant Rat: Fetal responses^1,2,

Foods and Nutrition Department, Purdue University, Lafayette, Indiana

Iron intake of rats fed pyridoxine and pyridoxine-deficient rats was approximately doubled by oral administration of FeSO₄ supplements containing 2 mg elemental iron daily during gestation. Effects of the treatments on the iron content of fetal plasma and tissue storage fractions were investigated. Fetuses of deficient mothers had low levels of plasma iron and transferrin and increased transferrin saturation. These changes were associated with increased concentrations of total iron, non-heme and hemosiderin components in the fetus. The overall effect of the deficiency appeared to be an increase in iron transfer from placental to fetal tissues, with some mitigation by the low levels of transferrin in fetal plasma and of ferritin in placenta. The inability of iron supplements, administered to mothers fed the vitamin, to increase the iron content of fetal plasma or tissues indicated that iron passage from the placenta to the fetus was regulated. This control mechanism appeared to be operative, at least in part, in pyridoxine deficiency since iron supplements administered to deficient mothers whose tissues were replete with iron did not result in increased fetal iron content. The decrease in placental total ferritin content in deficient and in iron-supplemented mothers is discussed in relation to the regulation.

² Supported in part by The Nutrition Foundation, Inc.

Manuscript received 21 March 1969.