Research Papers:

Maternal dietary zinc supplementation enhances the epigenetic-activated antioxidant ability of chick embryos from maternal normal and high temperatures

Yongwen Zhu _, Xiudong Liao, Lin Lu, Wenxiang Li, Liyang Zhang, Cheng Ji, Xi Lin, Hsiao-Ching Liu, Jack Odle and Xugang Luo

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Oncotarget. 2017; 8:19814-19824. https://doi.org/10.18632/oncotarget.15057

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Yongwen Zhu1,2,3,*, Xiudong Liao1,*, Lin Lu1, Wenxiang Li3, Liyang Zhang1, Cheng Ji3, Xi Lin4, Hsiao-Ching Liu4, Jack Odle4, Xugang Luo1

1Mineral Nutrition Research Division, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, P. R. China

2College of Animal Science, South China Agricultural University, Guangzhou 510000, P. R. China

3College of Animal Science and Technology, China Agricultural University, Beijing 100193, P. R. China

4Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA

*These authors have contributed equally to this work

Correspondence to:

Xugang Luo, email: [email protected]

Keywords: epigenetics, maternal hyperthermia, zinc, metallothionein, chick embryo

Received: October 29, 2016    Accepted: December 20, 2016    Published: February 03, 2017


The role of maternal dietary zinc supplementation in protecting the embryos from maternal hyperthermia-induced negative effects via epigenetic mechanisms was examined using an avian model (Gallus gallus). Broiler breeder hens were exposed to two maternal temperatures (21°C and 32°C) × three maternal dietary zinc treatments (zinc-unsupplemented control diet, the control diet + 110 mg zinc/kg inorganic or organic zinc) for 8 weeks. Maternal hyperthermia increased the embryonic mortality and induced oxidative damage evidenced by the elevated mRNA expressions of heat shock protein genes. Maternal dietary zinc deficiency damaged the embryonic development associated with the global DNA hypomethylation and histone 3 lysine 9 hyperacetylation in the embryonic liver. Supplementation of zinc in maternal diets effectively eliminated the embryonic mortality induced by maternal hyperthermia and enhanced antioxidant ability with the increased mRNA and protein expressions of metallothionein IV in the embryonic liver. The increased metallothionein IV mRNA expression was due to the reduced DNA methylation and increased histone 3 lysine 9 acetylation of the metallothionein IV promoter regardless of zinc source. These data demonstrate that maternal dietary zinc addition as an epigenetic modifier could protect the offspring embryonic development against maternal heat stress via enhancing the epigenetic-activated antioxidant ability.

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