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CPF Induces GC2spd Cell Injury via ROS/AKT/Efcab6 Pathway.

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Chlorpyrifos (CPF) pesticide exposure damages male reproductive cells by disrupting cell viability and inducing oxidative stress. This study reveals CPF causes male infertility via the ROS/AKT/Efcab6 pathway.

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Area of Science:

  • Environmental Toxicology
  • Reproductive Biology
  • Molecular Mechanisms

Background:

  • Chlorpyrifos (CPF) is a widely used insecticide with known reproductive toxicity.
  • Pesticide exposure presents growing concerns for male reproductive health.

Purpose of the Study:

  • To investigate the molecular mechanisms of male reproductive decline induced by Chlorpyrifos (CPF).
  • To identify potential therapeutic targets for CPF-induced male infertility.

Main Methods:

  • Utilized GC2spd cells for in vitro studies.
  • Employed flow cytometry, qRT-PCR, Western blot, RNA sequencing, and bioinformatics analysis.
  • Investigated the role of reactive oxygen species (ROS) and the ROS/AKT/Efcab6 pathway.

Main Results:

  • CPF significantly affected cell viability, cell cycle, apoptosis, and ROS accumulation in GC2spd cells.
  • RNA sequencing identified 626 differentially expressed genes, including Efcab6, Nox3, and Cmpk2.
  • CPF induces male reproductive damage through the ROS/AKT/Efcab6 pathway, involving PI3K-AKT signaling and glutamine metabolism.

Conclusions:

  • CPF exposure leads to male reproductive damage via the ROS/AKT/Efcab6 pathway.
  • Elucidates molecular targets and mechanisms for CPF-induced male infertility.
  • Provides a theoretical basis for preventing pesticide-induced reproductive harm.