AbstractPericonceptional Zn deprivation can affect development of 2‐ and 4‐cell mouse embryos in vitro as evidenced by fewer cells per embryo and delayed blastocyst development after 72 h in culture. One mechanism by which this could be occurring is through changes in oocyte and embryonic membrane structure/function. To test this idea,3H‐glycine uptake was measured in unfertilized oocytes and preimplantation embryos recovered from mice fed control ( + Zn; 50 μg Zn/g diet) or low Zn ( − Zn; ⩽O.4 μg Zn/g diet) diets for 6 days. In a second experiment, we assessed the in vitro development of preimplantation embryos in medium designed to inhibit cavitation through changes in membrane‐associated sodium flux. Preimplantation embryos from − Zn and + Zn mice recovered on day 1 of gestation were cultured in medium containing 147.2 mM sodium (normal) or 123 mM sodium (low sodium) for 48 h. In experiment 1, glycine uptake was similar in embryos from + Zn and − Zn mice, suggesting that the impaired in vitro development of embryos from − Zn mice is not due to gross changes in sodium‐dependent cell membrane function. In experiment 2, embryos recovered from − Zn mice and cultured in normal sodium medium contained fewer cells than controls. Embryos from both groups cultured in low sodium medium contained fewer cells than their normal sodium controls; the percent difference in cell number was 50 ± 8 and 56 ± 11 for embryos from + Zn and − Zn mice, respectively. The lack of an exacerbation of Zn deficiency‐induced impairment of in vitro development with the low sodium challenge further supports the idea that the reduction in embryonic cell number is not due to gross alterations in membrane structure and/or fu
展开▼
