INFLUENCE OF PERICONCEPTIONAL ZINC-DEFICIENCY ON EMBRYONIC PLASMA-MEMBRANE FUNCTION IN MICE

Periconceptional Zn deprivation can affect development of 2- and 4-cel l mouse embryos in vitro as evidenced by fewer cells per embryo and de layed blastocyst development after 72 h in culture. One mechanism by w hich this could be occurring is through changes in oocyte and embryoni c membrane structure/function. To test this idea, H-3-glycine uptake w as measured in unfertilized oocytes and preimplantation embryos recove red from mice fed control (+Zn; 50 mug Zn/g diet) or low Zn (-Zn; less -than-or-equal-to 0.4 mug Zn/g diet) diets for 6 days. In a second exp eriment, we assessed the in vitro development of preimplantation embry os in medium designed to inhibit cavitation through changes in membran e-associated sodium flux. Preimplantation embryos from -Zn and +Zn mic e recovered on day 1 of gestation were cultured in medium containing 1 47.2 mM sodium (normal) or 123 mM sodium (low sodium) for 48 h. In exp eriment 1, glycine uptake was similar in embryos from +Zn and -Zn mice , suggesting that the impaired in vitro development of embryos from -Z n mice is not due to gross changes in sodium-dependent cell membrane f unction. 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 t han their normal sodium controls; the percent difference in cell numbe r was 50 +/- 8% and 56 +/- 11% for embryos from +Zn and -Zn mice, resp ectively. The lack of an exacerbation of Zn deficiency-induced impairm ent of in vitro development with the low sodium challenge further supp orts the idea that the reduction in embryonic cell number is not due t o gross alterations in membrane structure and/or function.