Zinc is an essential component of over 300 proteins including antioxidants and zinc-binding factors which are required for a variety of biological mechanisms including cellular proliferation, differentiation and metabolism. Animal models of zinc-deficiency are consistently characterised by fetal growth restriction (FGR), however, the mechanisms behind this are unclear. We hypothesised that zinc deficiency results in increased oxidative stress (OS) within the placenta as well as reduced transfer of zinc to the fetuses contributing to FGR. In our mouse model, female mice received a quarter the amount of zinc in their diet compared to replete-fed controls throughout pregnancy. This resulted in a 26% decrease in maternal circulating zinc in the zinc-deficient animals and an 8% reduction in both fetal and placental weights near term compared to the controls (all P<0.05). Placental and fetal zinc however, remained similar between the control and zinc-deficient animals. There was an 18% increase in the number of cells which stained positive for 8-hydroxy-deoxy-guanosine, a marker of DNA damage caused by OS, in the placentas from the zinc-deficient animals. Microarray analysis and qPCR validation revealed a 1.9-fold increase in the expression of transferrin receptor (Tfrc) in placentas from the zinc-deficient animals (P<0.001) and this was associated with a 32% increase in Tfrc protein expression (P<0.05). This upregulation was likely in response to a 24% and 20% decrease in placental and fetal iron concentrations, respectively (both P<0.05) despite maternal circulating iron remaining similar between the zinc-deficient and control animals. These results show that zinc-deficiency in pregnancy results in increased OS within the placenta which may contribute to reduced fetal growth. Furthermore, a disruption to iron transport, possibly in order to conserve zinc in gestational tissues, may also be driving FGR in this model highlighting the importance of considering multiple micronutrient interactions when understanding the mechanisms of placental dysfunction.