College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, PR China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu, PR China.
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, PR China; Laboratory Animal Center, Xuzhou Medical University, Xuzhou, Jiangsu, PR China.
Ecotoxicol Environ Saf. 2021 Aug;219:112306. doi: 10.1016/j.ecoenv.2021.112306. Epub 2021 May 11.
Cadmium is an environmental pollutant that has extensive deleterious effects on the reproductive system. However, the mechanisms underlying the effects of cadmium on preimplantation embryos are unclear. Here, we used a mouse model to investigate the effects of maternal cadmium (32 mg/l) exposure in drinking water for 2 days on early embryonic development, and studied the mechanisms associated with epigenetic modifications and DNA damage induced by oxidative stress. We observed that maternal cadmium exposure impaired preimplantation embryo development by inducing embryo death, fragmentation, or developmental blockade. After cadmium exposure, the most survived embryos were at the 8-cell stage, which were used for all measurements. Histone acetylation, not methylation, was disturbed by increasing histone deacetylase 1 (HDAC1) levels after cadmium exposure. Cadmium also disrupted DNA methylation of H19; however genomic DNA methylation can be normally reprogrammed in embryos. Furthermore, cadmium increased reactive oxygen species (ROS) levels and DNA damage, and partly inhibited gene expression related to DNA repair. The distribution and activity of mitochondria was increased; therefore, embryos maintain intracellular homeostasis for survival. Collectively, our findings revealed that maternal cadmium exposure impairs preimplantation embryo development by disturbing the epigenetic modification and inducing DNA damage.
镉是一种环境污染物,对生殖系统有广泛的有害影响。然而,镉对着床前胚胎影响的机制尚不清楚。在这里,我们使用小鼠模型研究了母体镉(32mg/L)在饮用水中暴露 2 天对早期胚胎发育的影响,并研究了与氧化应激诱导的表观遗传修饰和 DNA 损伤相关的机制。我们观察到,母体镉暴露通过诱导胚胎死亡、碎片化或发育阻滞来损害着床前胚胎的发育。镉暴露后,最存活的胚胎处于 8 细胞期,用于所有测量。组蛋白去乙酰化酶 1(HDAC1)水平升高导致组蛋白乙酰化而非甲基化受到干扰。镉还破坏了 H19 的 DNA 甲基化;然而,基因组 DNA 甲基化可以在胚胎中正常重新编程。此外,镉增加了活性氧(ROS)水平和 DNA 损伤,并部分抑制了与 DNA 修复相关的基因表达。线粒体的分布和活性增加;因此,胚胎为了生存而保持细胞内的稳态。总之,我们的研究结果表明,母体镉暴露通过干扰表观遗传修饰和诱导 DNA 损伤来损害着床前胚胎的发育。