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

机译:母体膳食锌补充剂可增强母体正常和高温雏鸡胚胎的表观遗传激活的抗氧化能力

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摘要

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.
机译:使用禽类模型(Gallus gallus)检查了母体膳食锌补充剂通过表观遗传机制在保护胚胎免受母体热疗诱导的负面影响中的作用。肉鸡种鸡暴露于两种母体温度(21°C和32°C)×三种母体饮食锌处理(无锌对照饮食,对照饮食+ 110 mg锌/ kg无机或有机锌)8周。孕妇体温过高会增加胚胎死亡率,并引起氧化损伤,其表现为热休克蛋白基因mRNA表达的升高。母体饮食中锌缺乏会损害胚胎肝脏中与总体DNA甲基化不足和组蛋白3赖氨酸9过度乙酰化有关的胚胎发育。在母体饮食中补充锌有效消除了母体热疗所致的胚胎死亡率,并通过增加胚胎肝中金属硫蛋白IV的mRNA和蛋白表达而增强了抗氧化能力。金属硫蛋白IV mRNA表达的增加是由于金属硫蛋白IV启动子的DNA甲基化减少和组蛋白3赖氨酸9乙酰化增加,而与锌来源无关。这些数据表明,母亲饮食中添加锌作为表观遗传修饰剂可以通过增强表观遗传激活的抗氧化能力来保护后代胚胎发育免受母体热应激。

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