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Cleavage and Blastulation01:33

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Updated: May 16, 2025

Protocol for Human Blastoids Modeling Blastocyst Development and Implantation
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BPS causes abnormal blastocyst development by inhibiting cell proliferation.

Qing Liu1, Ruisong Bai1, Xiaoyu Zhang1

  • 1Anhui Province Key Laboratory of Embryo Development and Reproductive Regulation, Fuyang Normal University, Fuyang City, Anhui Province 236037, China.

Ecotoxicology and Environmental Safety
|April 3, 2025
PubMed
Summary
This summary is machine-generated.

Bisphenol S (BPS) exposure impairs early mouse embryonic development by disrupting cell cycle regulation and cell fate determination. This occurs through increased reactive oxygen species (ROS), not apoptosis, compromising blastocyst quality.

Keywords:
AutophagyBisphenol SCell proliferationImplantationMouse blastocyst

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Area of Science:

  • Reproductive Toxicology
  • Developmental Biology
  • Environmental Health

Background:

  • Global bisphenol S (BPS) use is increasing, raising health concerns.
  • BPS effects on mammalian embryonic development and mechanisms are poorly understood.

Purpose of the Study:

  • To investigate BPS toxicity during mouse embryogenesis.
  • To elucidate the molecular mechanisms of BPS-induced embryotoxicity.

Main Methods:

  • Mouse embryos were exposed to varying concentrations of BPS (0-25 μg/mL).
  • Evaluated embryonic quality, blastocyst formation, implantation potential, and cell number.
  • Assessed reactive oxygen species (ROS) levels, cell cycle, autophagy, and apoptosis (caspase 3/7 activity, TUNEL assay).

Main Results:

  • BPS exposure caused dose-dependent reductions in blastocyst formation and implantation potential.
  • Decreased total cell number and induced cell fate imbalance in blastocysts.
  • BPS elevated ROS, leading to cell cycle arrest and enhanced autophagy, independent of apoptosis.

Conclusions:

  • BPS disrupts early embryogenesis via ROS-mediated cell cycle dysregulation and impaired cell fate determination.
  • Compromised blastocyst developmental competence results from BPS exposure.
  • Identified novel mechanisms of BPS embryotoxicity for reproductive hazard assessment.