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<p>Polystyrene microplastics (PS-MPs), widely used in commercial and pharmaceutical products, are emerging endocrine-disrupting pollutants with potential reproductive toxicity. This study evaluated the dose-dependent effects of PS-MPs on adult male rats by assessing semen quality, reproductive hormones, oxidative stress, mitochondrial and inflammatory markers, and testicular histology. Rats were assigned to six groups: a control group and five groups receiving PS-MPs orally (0.1, 1, 10, 20, or 40&#xa0;µg/kg BW) for 45 days. PS-MP exposure reduced sperm count and motility, increased abnormal sperm, decreased testosterone, and elevated FSH and LH. Mitochondrial biogenesis/function markers (PGC-1α, UCP1, TFAM) were downregulated, while NF-κB, caspase-3, and TBARS were increased, accompanied by significant depletion of antioxidant defenses (GSH, GR, GPx, SOD, GST, CAT, TAC) and pronounced testicular histopathology. These effects were dose-dependent, and PS-MPs were detected in testicular tissue by pyrolysis-GC/MS at the doses of 10&#xa0;µg/kg and higher. Collectively, the data identify mitochondrial dysfunction–driven oxidative stress and associated inflammation as a key mechanism by which PS-MPs induce spermatogenic failure, hormonal disruption, and testicular damage, highlighting their potential as potent male reproductive toxicants.</p>

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Impact of polystyrene microplastic exposure at low doses on male fertility: an experimental study in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月23日

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  • Aisha H. A. Alsenousy,
  • Asmaa Hassan Younis Khalaf,
  • Hesham Zaki Ibrahim,
  • Maher A. Kamel,
  • Mokhtar Ibrahim Yousef

摘要

Polystyrene microplastics (PS-MPs), widely used in commercial and pharmaceutical products, are emerging endocrine-disrupting pollutants with potential reproductive toxicity. This study evaluated the dose-dependent effects of PS-MPs on adult male rats by assessing semen quality, reproductive hormones, oxidative stress, mitochondrial and inflammatory markers, and testicular histology. Rats were assigned to six groups: a control group and five groups receiving PS-MPs orally (0.1, 1, 10, 20, or 40 µg/kg BW) for 45 days. PS-MP exposure reduced sperm count and motility, increased abnormal sperm, decreased testosterone, and elevated FSH and LH. Mitochondrial biogenesis/function markers (PGC-1α, UCP1, TFAM) were downregulated, while NF-κB, caspase-3, and TBARS were increased, accompanied by significant depletion of antioxidant defenses (GSH, GR, GPx, SOD, GST, CAT, TAC) and pronounced testicular histopathology. These effects were dose-dependent, and PS-MPs were detected in testicular tissue by pyrolysis-GC/MS at the doses of 10 µg/kg and higher. Collectively, the data identify mitochondrial dysfunction–driven oxidative stress and associated inflammation as a key mechanism by which PS-MPs induce spermatogenic failure, hormonal disruption, and testicular damage, highlighting their potential as potent male reproductive toxicants.