Abstract
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.
Highlights
Maternal heat stress impairs the fetal and embryonic development in mammalian and avian species [1, 2]
We have demonstrated that dietary www.impactjournals.com/oncotarget supplementation with Zn increased mRNA and protein expressions of tissue metallothionein (MT) as free radical scavengers in broilers [12,13,14]
Lipid peroxidation was not observed in the www.impactjournals.com/oncotarget livers of maternal heat-stressed embryos based on MDA content
Summary
Maternal heat stress impairs the fetal and embryonic development in mammalian and avian species [1, 2]. Lower levels of global DNA methylation and histone acetylation from maternal stress contributed to the abnormal development and embryo death in mice and human [6, 7]. The disruption of embryonic development due to Zn deficiency was associated with epigenetic defects such as the reduced methylation levels of DNA and histones, and these impairments were restored by dietary methyl donor supplementation [9]. Prenatal Zn deficiency increased MT2 promoter DNA methylation and histone acetylation levels in liver of offspring mice [15]. The hypothesis of the present study was to investigate whether maternal dietary supplementations with different Zn sources could protect offspring chick embryos against the maternal hyperthermia-induced oxidative damage via epigenetic activation of MT4 expression
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