Response of Mouse Zygotes Treated with Mild Hydrogen Peroxide as a Model to Reveal Novel Mechanisms of Oxidative Stress-Induced Injury in Early Embryos.

Response of Mouse Zygotes Treated with Mild Hydrogen Peroxide as a Model to Reveal Novel Mechanisms of Oxidative Stress-Induced Injury in Early Embryos.
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以轻度过氧化氢处理的小鼠受精卵的反应为模型,揭示早期胚胎氧化应激损伤的新机制

DOI:
10.1155/2016/1521428
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发表时间:
2016
影响因子:
--
通讯作者:
Wang B
Wang B
中科院分区:
生物学2区
文献类型:
--
作者:
Qian D;Li Z;Zhang Y;Huang Y;Wu Q;Ru G;Chen M;Wang B

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我们的研究旨在开发胚胎模型来评估氧化应激对胚胎发育的影响。实验1中,将处于G1期的小鼠受精卵用准备好的培养基(含有0.00、0.01、0.02、0.03、0.04、0.05或0.1 mM过氧化氢(H2O2))处理30分钟。通过比较每个阶段(2细胞和4细胞)的形成率,研究H2O2对胚胎发育的剂量效应。胚胎和囊胚)。实验 2 的目的是比较轻度氧化应激状态 (0.03 mM H2O2) 下的胚胎与对照组 (0 mM H2O2) 下的胚胎行为。检测活性氧(ROS)水平、线粒体膜电位(MMP)变化、γH2AX表达以及囊胚细胞凋亡率。我们观察到卵裂率和囊胚率呈剂量依赖性下降。此外,较高水平的ROS、快速减少的MMP以及γH2AX的出现表明胚胎在轻度氧化应激下早期受到损伤。此外,γH2AX 可能参与早期胚胎的 DNA 损伤反应。当DNA损伤修复不充分时,囊胚的凋亡率可能显着增加。最重要的是,我们的研究提供了胚胎模型来研究不同水平氧化应激条件下的细胞周期调控和DNA损伤反应。
Our study aimed to develop embryo models to evaluate the impact of oxidative stress on embryo development. Mouse zygotes, which stayed at G1 phase, were treated with prepared culture medium (containing 0.00, 0.01, 0.02, 0.03, 0.04, 0.05, or 0.1 mM hydrogen peroxide (H2O2)) for 30 min in experiment 1. The dose‐effects of H2O2 on embryo development were investigated via comparisons of the formation rate at each stage (2‐ and 4‐cell embryos and blastocysts). Experiment 2 was carried out to compare behaviors of embryos in a mild oxidative‐stressed status (0.03 mM H2O2) with those in a control (0 mM H2O2). Reactive oxygen species (ROS) levels, variation of mitochondrial membrane potential (MMP), expression of γH2AX, and cell apoptosis rate of blastocyst were detected. We observed a dose‐dependent decrease on cleavage and blastocyst rates. Besides, higher level of ROS, rapid reduction of MMP, and the appearance of γH2AX revealed that embryos are injured early in mild oxidative stress. Additionally, γH2AX may involve during DNA damage response in early embryos. And the apoptotic rate of blastocyst may significantly increase when DNA damage repair is inadequate. Most importantly, our research provides embryo models to study cell cycle regulation and DNA damage response under condition of different levels of oxidative stress.
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