Polystyrene microplastics induce blood-testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats

Shengda Li1, Qimeng Wang1, Hui Yu2

  • 1College of Clinical Medicine, Binzhou Medical University, Yan Tai, People's Republic of China.

Insights

Polystyrene microplastics (PS-MPs) harm male rat reproduction by damaging sperm and impairing the blood-testis barrier (BTB). This occurs via oxidative stress and the MAPK-Nrf2 pathway, leading to spermatogenic cell apoptosis.

Area of Science:

  • Environmental Toxicology
  • Reproductive Biology
  • Cellular Mechanisms

Background:

  • Microplastics (MPs) are persistent pollutants with known effects on male fertility.
  • The precise mechanisms by which MPs, specifically polystyrene microplastics (PS-MPs), impact male reproductive health and the blood-testis barrier (BTB) remain largely unknown.

Purpose of the Study:

  • To investigate the effects of PS-MPs on male rat reproductive parameters.
  • To elucidate the underlying mechanisms of PS-MP-induced BTB impairment and male reproductive toxicity.

Main Methods:

  • Adult male Wistar rats were exposed to varying doses of PS-MPs (0, 0.015, 0.15, 1.5 mg/day) for 90 days.
  • Evaluated were seminiferous tubule integrity, spermatogenic cell apoptosis, sperm count, motility, and morphology.
  • Investigated were oxidative stress markers, the p38 MAPK pathway, Nrf2 levels, and BTB-related protein expression.

Main Results:

  • PS-MP exposure caused seminiferous tubule damage, increased spermatogenic cell apoptosis, and reduced sperm motility and concentration.
  • Sperm abnormalities were elevated, alongside induced oxidative stress and activation of the p38 MAPK pathway, leading to Nrf2 depletion.
  • PS-MPs significantly decreased the expression of BTB-related proteins.

Conclusions:

  • PS-MP exposure induces male reproductive toxicity in rats.
  • The mechanism involves oxidative stress, p38 MAPK pathway activation, Nrf2 depletion, and subsequent BTB destruction and spermatogenic cell apoptosis.

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