Influence of periconceptional zinc deficiency on embryonic plasma membrane function in mice

Periconceptional 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 micrograms Zn/g diet) or low Zn (-Zn; < or = 0.4 micrograms 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.(ABSTRACT TRUNCATED AT 250 WORDS)