Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model.

Wei Gao,Chuang Liu,Liang Huang,Yaohui Zheng,Wence Wang,Yongwen Zhu,Shi Wei,Xiufen Zhang,Xinyan Ma,Wei Geng,Lin Yang,Carla Tatone

doi:10.1155/2021/9013280

Abstract

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.

Highlights

Zinc (Zn) is an essential trace mineral required for maintaining the normal growth and development of embryos [1]
Alkaline phosphatase (ALP) is a Zn metalloenzyme, and its activity in blood was decreased by 80% when the Zn content was reduced from 96 mg/kg to 1.2 mg/kg in the rat [7]
It is speculated that the activities of ALP and 5′-NT could be developed as specific sensitive biomarkers for predicting the marginal Zn-deficient status

Summary

Introduction

Zinc (Zn) is an essential trace mineral required for maintaining the normal growth and development of embryos [1]. Severe Zn deficiency in maternal diets resulted in growth retardation, abnormal development, and increased mortality of embryos [3]. It is crucial to assess or predict maternal marginal Zn nutritional status to prevent embryos subjected to severe Zn deficiency. It is necessary to select some specific sensitive biomarkers to predict maternal marginal Zn status. Some studies in rats and humans revealed that plasma Zn concentration could be used as a sensitive biomarker in response to Zn status [5, 6]. The 5′-nucleotidase (5′-NT) activity, like a cell membrane enzyme in erythrocyte and thymulin [8], was more sensitive to mild Zn deficiency than plasma Zn concentration [9, 10]. It is speculated that the activities of ALP and 5′-NT could be developed as specific sensitive biomarkers for predicting the marginal Zn-deficient status

Objectives

Methods

Results

Discussion

Conclusion