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Polystyrene microplastics trigger testosterone decline via GPX1.

Jiayuan Qu1, Liling Wu1, Li Mou1

  • 1NHC Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning Science and Technology Research Institute, Chongqing 401120, PR China.

The Science of the Total Environment
|July 8, 2024
PubMed
Summary
This summary is machine-generated.

Polystyrene microplastics (PS-MPs) harm male reproduction by disrupting testosterone synthesis. These microplastics accumulate in testes, reduce Leydig cell viability, and trigger oxidative and endoplasmic reticulum stress, leading to lower testosterone levels.

Keywords:
GPX1PERK-EIF2α-ATF4-CHOP pathwayPolystyrene microplasticsTestosterone declineUbiquitination

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Area of Science:

  • Environmental Science
  • Toxicology
  • Reproductive Biology

Background:

  • Polystyrene microplastics (PS-MPs) are emerging environmental contaminants.
  • PS-MPs are suspected endocrine disruptors with anti-androgenic properties.
  • Adverse effects on male reproductive function are a growing concern.

Purpose of the Study:

  • To investigate the adverse effects of PS-MPs on testosterone synthesis and male reproduction.
  • To elucidate the underlying mechanisms of PS-MP-induced reproductive damage.
  • To assess the role of oxidative and endoplasmic reticulum stress pathways.

Main Methods:

  • Exposure of BALB/c mice and Leydig cells to 50 μm PS-MPs.
  • Histomorphological and ultrastructural analysis of testicular tissue.
  • Measurement of serum hormone levels (GnRH, FSH, LH, testosterone).
  • Investigation of molecular pathways including ubiquitination, miR-425-3p, GPX1, and ER stress (PERK-EIF2α-ATF4-CHOP).

Main Results:

  • PS-MPs accumulated in mouse testes and Leydig cells, causing damage.
  • Reduced Leydig cell viability and suppressed serum hormone levels observed.
  • PS-MPs induced oxidative stress via GPX1 suppression.
  • Endoplasmic reticulum stress pathway (PERK-EIF2α-ATF4-CHOP) was activated.
  • CHOP upregulated SRD5A2, accelerating testosterone metabolism.
  • Interference with the hypothalamic-pituitary-testis (HPT) axis noted.

Conclusions:

  • PS-MPs exhibit anti-androgenic characteristics and impair male reproductive function.
  • GPX1 plays a critical role in PS-MP-induced testosterone decline.
  • PS-MPs disrupt testosterone homeostasis through multiple molecular pathways.