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Biol Reprod. 2014 Apr 25;90(4):83. doi: 10.1095/biolreprod.113.113910. Print 2014 Apr.

Preconception zinc deficiency disrupts postimplantation fetal and placental development in mice.

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Center for Reproductive Biology and Health and Department of Animal Science, Pennsylvania State University, University Park, Pennsylvania.


Zinc is an essential nutrient for optimal fertility, but the effects of preconception zinc deficiency on postimplantation development are not known. Female mice were fed a control or a zinc-deficient diet (ZDD) for 4-5 days before ovulation (preconception). Embryonic and/or placental development were evaluated on Days 3.5, 6.5, 10.5, 12.5, and 16.5 of pregnancy. The findings show a decrease in embryo length (31%, Day 10.5; 13%, Day 12.5; 10%, Day 16.5) and weight (23%, Day 16.5) in embryos from mothers fed a ZDD preconception. Zinc deficiency also caused a high incidence of pregnancy loss (46%, Day 10.5; 34%, Day 12.5; 51%, Day 16.5) compared to control (2%, Day 10.5; 7%, Day 12.5; 9%, Day 16.5). ZDD embryos transferred to normal recipients were 38% smaller and implantation rate was only 10% compared to 40% for controls. Trophoblast cell differentiation and implantation on Day 6.5 of pregnancy were compromised by preconception zinc deficiency. On Day 12.5 of pregnancy, placenta weight and area of fetal placenta were decreased 37% and 31%, respectively, by preconception zinc deficiency. Consistent with a smaller fetal placenta, expression of key placental transcripts, including Ar, Esx1, Syna, Tfeb, Dlx3, and Gcm1 mRNA, but not Ctsq mRNA, were decreased 30%-70% in the ZDD group. Preconception zinc deficiency caused 41%-57% of embryos to exhibit delayed or aberrant neural tube development, as examined by light microscopy and magnetic resonance imaging. Collectively, the findings provide evidence for the importance of preconception zinc in promoting optimal fertility and oocyte developmental potential.


fetal development; oocyte; zinc

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