2017 journal article

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

ONCOTARGET, 8(12), 19814–19824.

By: Y. Zhu *, X. Liao *, L. Lu *, W. Li *, L. Zhang *, C. Ji*, . Lin  n, H. Liu n, J. Odle n , X. Luo*

author keywords: epigenetics; maternal hyperthermia; zinc; metallothionein; chick embryo
MeSH headings : Acetylation / drug effects; Animal Nutritional Physiological Phenomena; Animals; Antioxidants / metabolism; Avian Proteins / genetics; Avian Proteins / metabolism; Blotting, Western; Chick Embryo; Chickens; DNA Methylation / drug effects; Dietary Supplements; Epigenesis, Genetic / drug effects; Female; Gene Expression Regulation, Developmental / drug effects; Heat-Shock Proteins / genetics; Heat-Shock Proteins / metabolism; Histones / metabolism; Hot Temperature; Liver / drug effects; Liver / embryology; Liver / metabolism; Lysine / metabolism; Metallothionein / genetics; Metallothionein / metabolism; Reverse Transcriptase Polymerase Chain Reaction; Zinc / administration & dosage; Zinc / pharmacology
TL;DR: It is demonstrated 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. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

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.