Teratogenic effects of short‐term and transitory zinc deficiency in rats

Abstract

Abstract Female rats fed a zinc‐deficient diet during pregnancy (days 0 to 21) had impaired reproduction and a high incidence of congenitally malformed young even though they had been fed a normal diet adequate in zinc until the beginning of gestation. With a deficiency from days 0 to 21 of pregnancy 41% of the implantation sites were resorbed, full‐term young weighed about half that of controls, and 90% of the fetuses showed gross malformations affecting every organ system. These results were similar to those found previously with females fed a zinc‐low diet from weaning. The fetal malformations were specifically due to a maternal dietary deficiency of zinc rather than to reduced food intake since females fed restricted amounts of a zinc‐supplemented diet had normal young. Shorter periods of deficiency were also teratogenic. With a deficiency from days 0 to 10 of pregnancy 22% of the young were malformed, and from days 0 to 12, 56% were malformed. When the zinc‐deficient regime was imposed from days 6 to 14 of pregnancy almost half of the young were abnormal. Transitory periods of deficiency altered the incidences of the anomalies observed in accordance with the developmental events occurring at the time the deficiency was imposed. The rapid and severe effects of even relatively short periods of zinc deficiency on fetal development suggest that the pregnant rat cannot mobilize zinc from body stores in amounts sufficient to supply the needs of developing fetuses.