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<p>Acrylamide is a synthetic material which is widely used in water treatment and paper manufacturing, and it is also generated from food formation, which shows neurological effects, skin irritation, or reproductive toxicity. Several studies focused on the effects of acrylamide on mitochondria and apoptosis in oocytes. In present study, we reported that acrylamide disturbed cell cycle progression of mouse oocyte meiosis. Our data showed that acrylamide caused both germinal vesicle (GV) breakdown and polar body extrusion defects. Further analysis indicated that acrylamide induced DNA damage in the GV oocytes, showing with increased γ-H2A.X expression, which active CHK2 for G2/M transition. This could be confirmed by the altered Cyclin B1 and CDK1 expression in oocytes. Besides, we found kinetochore-microtubule attachment was aberrant in metaphase I (MI) oocytes, which active spindle assembly checkpoint (SAC) for polar body extrusion, and this was confirmed by the consistent presentence of BubR1 and Bub3. This was due to the reduced tubulin acetylation-based microtubule stability, since HDAC6 and NAT10 expression was changed and cold treatment reduced the tubulin polymerization. Taken together, our study reported that acrylamide exposure disrupted cell cycle progression through DNA damage-based MPF activity and tubulin acetylation-based SAC activation in oocytes.</p>

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Acrylamide disrupts meiotic G2/M transition and SAC activity during oocyte maturation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月30日

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  • Shanshan Chen,
  • Peng-Xia Wang,
  • Yan-Ting Wang,
  • Xing-He Ke,
  • Minmin Ou,
  • Shao-Chen Sun,
  • Bi-Yun Liao,
  • Xuanyi Chen

摘要

Acrylamide is a synthetic material which is widely used in water treatment and paper manufacturing, and it is also generated from food formation, which shows neurological effects, skin irritation, or reproductive toxicity. Several studies focused on the effects of acrylamide on mitochondria and apoptosis in oocytes. In present study, we reported that acrylamide disturbed cell cycle progression of mouse oocyte meiosis. Our data showed that acrylamide caused both germinal vesicle (GV) breakdown and polar body extrusion defects. Further analysis indicated that acrylamide induced DNA damage in the GV oocytes, showing with increased γ-H2A.X expression, which active CHK2 for G2/M transition. This could be confirmed by the altered Cyclin B1 and CDK1 expression in oocytes. Besides, we found kinetochore-microtubule attachment was aberrant in metaphase I (MI) oocytes, which active spindle assembly checkpoint (SAC) for polar body extrusion, and this was confirmed by the consistent presentence of BubR1 and Bub3. This was due to the reduced tubulin acetylation-based microtubule stability, since HDAC6 and NAT10 expression was changed and cold treatment reduced the tubulin polymerization. Taken together, our study reported that acrylamide exposure disrupted cell cycle progression through DNA damage-based MPF activity and tubulin acetylation-based SAC activation in oocytes.