Severe maternal zinc deficiency has a devastating effect on pregnancy outcome. Studies of humans and experimental animals show that maternal zinc deficiency can cause infertility, prolonged labor, intrauterine growth retardation, teratogenesis, severe immunological deficiencies, or fetal death. The additional need for zinc during pregnancy can be met by an increase in zinc intake. An increase in zinc supplements, when excessive, can cause a decrease in copper. Therefore, it is important to determine the zinc and copper concentrations in embryonic tissue in experimental models and their relationship with embryo number and viability. BALB/c mice were divided into groups according to zinc oral supplementation and gestational age. Phagocytosis was assessed in peritoneal macrophages from dams. The zinc and copper concentrations were obtained by inductively coupled plasma-optical emission spectrometry. Zn and Cu data concentrations in all the analyzed samples were above the detection limits. No spectral interferences were found in both elements. Zinc concentrations show a tendency to increase in embryos (14 gestational days and 21 gestational days) supplemented with zinc. Copper concentrations showed a noticeable tendency to diminish (36% and 27%, respectively) in the same period. In contrast, in placenta Zn values were increased by 30% and Cu values were decreased by 26%. We suggest a pivotal role of the placenta metabolism with its homeostatic mechanisms, in these findings. An important increment appeared in the +Zn embryo number (40%) relative to control (-Zn) embryos at 21 d gestational age. Embryo mortality was at 6% in +Zn embryos and at 20% in -Zn embryos. We consider these findings, both in the number and in the viability of +Zn embryos, outstanding.