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Pyridoxine Deficiency and Iron Metabolism in the Pregnant Rat: Maternal Responses¹

Foods and Nutrition Department, Purdue University, Lafayette, Indiana

Effects of pyridoxine deficiency on the normal increase in iron absorption in the pregnant rat and on the use of a large dose of iron administered orally during gestation were investigated. The deficiency was evidenced by poor reproductive performance and impaired erythropoiesis, including polycythemia and reduced mean corpuscular hemoglobin and mean corpuscular volume. Plasma iron concentration, total iron-binding capacity and unsaturated iron-binding capacity were not altered in deficient animals even in those receiving large doses of iron. During normal gestation iron was mobilized from spleen stores and small amounts from liver. Iron supplementation alleviated the reduction in liver stores but had little effect on spleen. Elevation in liver iron observed in the deficiency was more pronounced in nonpregnant than pregnant animals. Similarly iron supplements intensified elevations more in nonpregnant than pregnant animals. Differences were related to use of maternal stores for fetal needs. Spleen values elevated in the deficiency were not intensified by iron supplements or by pregnancy. Elevations were related in part to less utilization of iron in erythropoiesis. Hemosiderin-to-ferritin ratios were increased in liver, spleen and duodenal tissues of deficient animals. Although alterations in tissue iron stores were observed in the deficiency, no major impairment in iron absorption appeared evident. Deficient animals tolerated large doses of oral iron during gestation when iron absorption is normally increased.

Manuscript received 19 January 1967.