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<p>Environmental toxicants pose a significant threat to female reproductive health, yet the molecular mechanisms through which they impair oocyte quality are often unclear. Although the industrial chemical 4-vinylcyclohexene diepoxide (VCD) is known to cause ovarian follicle loss, how it disrupts essential processes such as meiosis remains poorly understood. Here, we show that VCD exposure triggers meiotic failure in mouse oocytes by altering a key RNA modification pathway known as m6A methylation. VCD treatment reduces ovarian reserve, elevates oxidative stress, and causes severe chromosome segregation defects. We find that VCD dysregulates the expression of m6A writers and erasers, leading to altered methylation of transcripts critical for cell division and meiosis. Specifically, VCD downregulates the RNA-binding protein IGF2BP3, which destabilizes target genes required for chromosome alignment and spindle assembly. Our results reveal how an environmental toxin can cause epitranscriptomic dysregulation and meiotic failure, providing a new perspective on pollutant-induced fertility decline. This work highlights the m6A pathway as a potential therapeutic target and underscores the broader reproductive risks posed by chemical exposures.</p><p></p>

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Ovotoxicant VCD disrupts oocyte meiosis in mice by impairing m6A/IGF2BP3-mediated mRNA stability

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月27日

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  • Yang Li,
  • Yuling Zhou,
  • Jian Liu,
  • Guangning Nie,
  • Fangping Cheng,
  • Hongyan Yang

摘要

Environmental toxicants pose a significant threat to female reproductive health, yet the molecular mechanisms through which they impair oocyte quality are often unclear. Although the industrial chemical 4-vinylcyclohexene diepoxide (VCD) is known to cause ovarian follicle loss, how it disrupts essential processes such as meiosis remains poorly understood. Here, we show that VCD exposure triggers meiotic failure in mouse oocytes by altering a key RNA modification pathway known as m6A methylation. VCD treatment reduces ovarian reserve, elevates oxidative stress, and causes severe chromosome segregation defects. We find that VCD dysregulates the expression of m6A writers and erasers, leading to altered methylation of transcripts critical for cell division and meiosis. Specifically, VCD downregulates the RNA-binding protein IGF2BP3, which destabilizes target genes required for chromosome alignment and spindle assembly. Our results reveal how an environmental toxin can cause epitranscriptomic dysregulation and meiotic failure, providing a new perspective on pollutant-induced fertility decline. This work highlights the m6A pathway as a potential therapeutic target and underscores the broader reproductive risks posed by chemical exposures.