Scholarlink

<p>Environmental constant light exposure could induce biological rhythm disruption, which negatively induces metabolic syndrome, mood disorders, cognitive declines, chronic disease risk, and reproduction defects. Previous studies indicated that constant light exposure affected ovary function and oocyte quality. Here, we reported that melatonin supplementation effectively alleviated the adverse effects of constant light exposure on embryonic development by improving oocyte quality. Our results showed that constant light exposure reduced blastocyst formation during mouse embryo development, and the levels of DNA and histone methylation modifications of embryos were altered. This might be due to the low oocyte quality since we observed aberrant spindle formation, which might be caused by HDAC6-medicated tubulin acetylation for microtubule stability, and this further induced K-MT attachment defects for aneuploidy. Besides, spindle migration was disturbed due to ARP2-based actin assembly defects. Light exposure also led to oocyte elevated ROS level, DNA damage, and then activated LC3-based autophagy and disrupted lysosome function. Notably, in vivo melatonin supplementation effectively rescued these defects in the oocytes and embryos of the mice under constant light exposure. Collectively, our results suggested that melatonin preserved embryo development potential and epigenetic modifications under constant light exposure by maintaining oocyte redox homeostasis and cytoskeletal dynamics.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Constant light exposure impairs embryonic development via disrupting oocyte cytoskeleton integrity and redox homeostasis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月24日

查看全文
  • Ping-Shuang Lu,
  • Zi-Jian Wu,
  • Si-Le Wu,
  • Meng-Xiang Li,
  • Lin-Lin Hu,
  • Bi-Yun Liao,
  • Jinhui Shu,
  • Caizhu Wang,
  • Shao-Chen Sun

摘要

Environmental constant light exposure could induce biological rhythm disruption, which negatively induces metabolic syndrome, mood disorders, cognitive declines, chronic disease risk, and reproduction defects. Previous studies indicated that constant light exposure affected ovary function and oocyte quality. Here, we reported that melatonin supplementation effectively alleviated the adverse effects of constant light exposure on embryonic development by improving oocyte quality. Our results showed that constant light exposure reduced blastocyst formation during mouse embryo development, and the levels of DNA and histone methylation modifications of embryos were altered. This might be due to the low oocyte quality since we observed aberrant spindle formation, which might be caused by HDAC6-medicated tubulin acetylation for microtubule stability, and this further induced K-MT attachment defects for aneuploidy. Besides, spindle migration was disturbed due to ARP2-based actin assembly defects. Light exposure also led to oocyte elevated ROS level, DNA damage, and then activated LC3-based autophagy and disrupted lysosome function. Notably, in vivo melatonin supplementation effectively rescued these defects in the oocytes and embryos of the mice under constant light exposure. Collectively, our results suggested that melatonin preserved embryo development potential and epigenetic modifications under constant light exposure by maintaining oocyte redox homeostasis and cytoskeletal dynamics.