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Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model
- Source :
- Oxidative Medicine and Cellular Longevity, Oxidative Medicine and Cellular Longevity, Vol 2021 (2021)
- Publication Year :
- 2021
- Publisher :
- Hindawi Limited, 2021.
-
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.
- Subjects :
- Aging
Embryo, Nonmammalian
Erythrocytes
Antioxidant
Article Subject
medicine.medical_treatment
Nutritional Status
chemistry.chemical_element
Apoptosis
Zinc
Biology
behavioral disciplines and activities
Biochemistry
Andrology
chemistry.chemical_compound
Nucleotidase
medicine
Animals
5'-Nucleotidase
QH573-671
Superoxide
Embryogenesis
Gene Expression Regulation, Developmental
Maternal Nutritional Physiological Phenomena
Cell Biology
General Medicine
medicine.disease
Disease Models, Animal
Oxidative Stress
Ducks
Liver
chemistry
Zinc deficiency
Alkaline phosphatase
Female
Cytology
Apoptosis Regulatory Proteins
Deficiency Diseases
Oxidation-Reduction
Research Article
Subjects
Details
- ISSN :
- 19420994 and 19420900
- Volume :
- 2021
- Database :
- OpenAIRE
- Journal :
- Oxidative Medicine and Cellular Longevity
- Accession number :
- edsair.doi.dedup.....08b3145cba61ee11365301dc2ae1219c