Maternal severe zinc (Zn) deficiency resulted in growth retardation and high mortality during embryonic development in human. Therefore, this study is aimed at evaluating the effect of maternal marginal Zn deficiency on the development and redox status to avoid severe Zn deficiency using an avian model. A total of 324 laying duck breeders at 214 days old were randomly allotted into 3 dietary Zn levels with 6 replicates of 18 ducks per replicate. The birds were fed experimental diets including 3 dietary supplemental Zn levels of 0 mg/kg (maternal Zn-deficient group, 29.2 mg Zn/kg diet), 60 mg/kg (maternal Zn-adequate group), and 120 mg/kg (maternal Zn-high group) for 6 weeks. Dietary Zn levels had on effect on egg production and fertility ( P > 0.05 ), whereas dietary Zn deficiency decreased breeder plasma Zn concentration and erythrocytic alkaline phosphatase activity at week 6 and inhibited erythrocytic 5 ′ -nucleotidase (5 ′ -NT) activity at weeks 2, 4, and 6 ( P < 0.05 ), indicating that marginal Zn-deficient status occurred after Zn depletion. Maternal marginal Zn deficiency increased embryonic mortality and contents of superoxide anion radical, MDA, and PPC and reduced MT content and CuZnSOD activity in duck embryonic livers on E29. The MDA content was positively correlated with embryonic mortality. Maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expressions as well as decreased B-cell lymphoma-2 and MT1 mRNA and signal AKT1 and ERK1 protein expressions ( P < 0.05 ). Breeder plasma Zn concentration and erythrocytic 5 ′ -NT activities at week 6 were positively correlated with GSH-Px activity and GPx, MT1, and BCL2 mRNA expressions in embryonic livers on E29. In conclusion, erythrocytic 5 ′ -NT activity could be more rapid and reliable to monitor marginal Zn-deficient status. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced oxidative damage and apoptosis in the embryonic liver, contributing to the greater loss of duck embryonic death.

BackgroundMaternal severe zinc (Zn) deficiency induced oxidative damage and apoptosis in embryos, resulting in growth retardation. Therefore, it is crucial to assess maternal marginal Zn nutritional status for poultry breeders to prevent embryos subjected to severe Zn deficiency. MethodsIn Exp. 1, twelve egg embryos were sampled at incubation day 17 (E17), E20, E23, E26, E29, and E32 (day of hatch) respectively, with 6 replicates of 2 embryo each. The developmental changes of Zn mobilization and Zn transport gene mRNA expression were determined. In Exp. 2, 324 laying duck breeders were randomly allotted into 3 dietary Zn levels (0, 60, and 120 mg Zn/kg diet) with 6 replicates of 18 ducks per replicate. Plasma Zn concentration and erythrocytic Zn metalloenzyme activities in breeders as well as the development, redox status, and gene expression related to oxidation and apoptosis in embryos were measured. Blood samples were collected at the 2th, 4th and 6th weeks of the experiment. ResultsIn Exp. 1, the overall Zn mobilization rates were increased in yolk sac and embryonic liver in response to the increased incubation period, associated with the decreased ZIP10, 13, and 14 mRNA expressions in embryonic liver (P < 0.05). In Exp. 2, with the prolonged dietary Zn depletion, maternal Zn deficiency decreased plasma Zn concentration and erythrocytic alkaline phosphatase activity at the 6th week and inhibited erythrocytic 5'-nucleotidase (5’-NT) activity at 2th week (P < 0.05). On E29 of the maximal rate of Zn mobilization, maternal marginal Zn deficiency increased middle and late embryonic mortality and contents of superoxide anion radical, MDA and PPC, as well as decreasedMT content, CuZnSOD activity, and MT1 mRNA expression in embryonic livers (P < 0.05). Additionally, maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expression and decreased B-cell lymphoma-2 mRNA expression in embryonic liver (P < 0.05). ConclusionErythrocytic 5’-NT activity was more rapid and reliable to assess marginal Zn-deficient status in duck breeders. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced the oxidative damage and apoptosis in embryonic liver, contributing to the greater loss of embryonic death.