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Chronic exposure to polystyrene micro/nanoplastics triggers testicular dysfunction through PI3K/AKT/mTOR
Huilian Zhang1, Yi Li1, Nan Zhu1
1School of Public Health, Chongqing Medical University, Chongqing, 400016, China; Joint International Research Laboratory of Reproduction and Development of the Ministry of Education, Chongqing, 400016, China.
Abstract:
While the potential microplastic toxicity has attracted considerable research attention, studies on its chronic reproductive effects in male mammals remain limited. Here, we investigated the chronic reproductive toxicity of polystyrene microplastics (PS-MPs, 5 μm) and polystyrene nanoplastics (PS-NPs, 20 nm) both in vitro, using GC2 cells, and in vivo, employing male C57 mice. Histopathological analysis revealed dilated seminiferous tubules, disorganized spermatocytes, and reduced spermatocyte counts in treated groups. Consistently, sperm count and motility were significantly decreased following PS-MPs and PS-NPs exposure. These effects were closely associated with spermatocyte senescence, as indicated by β-galactosidase activity and the markers of telomerase inhibition, DNA damage, and cell cycle arrest. Mechanistically, PS-MPs and PS-NPs trigger spermatocyte senescence through activation of the PI3K/AKT/mTOR signaling pathway. Our findings demonstrate that PS-MPs and PS-NPs cause structural damage and spermatogenic dysfunction in mouse testes, potentially mediated by spermatocyte senescence through the PI3K/AKT/mTOR pathway.
Insights
Polystyrene microplastics and nanoplastics harm male fertility by damaging testes and reducing sperm count and motility. This reproductive toxicity is linked to cell aging and the PI3K/AKT/mTOR pathway.
Area of Science:
- Environmental Toxicology
- Reproductive Biology
- Nanotechnology
Background:
- Microplastic toxicity is a growing concern, yet chronic reproductive effects in male mammals are understudied.
- Polystyrene microplastics (PS-MPs) and nanoplastics (PS-NPs) are common environmental contaminants.
- Understanding their impact on male reproductive health is crucial.
Purpose of the Study:
- To investigate the chronic reproductive toxicity of PS-MPs and PS-NPs in male mice.
- To explore the underlying mechanisms, including spermatocyte senescence and signaling pathways.
Main Methods:
- In vitro studies using GC2 cells and in vivo studies using male C57 mice.
- Histopathological analysis of testicular tissue.
- Assessment of sperm parameters (count, motility).
- Evaluation of spermatocyte senescence markers (β-galactosidase, telomerase inhibition, DNA damage, cell cycle arrest).
- Investigation of the PI3K/AKT/mTOR signaling pathway.
Main Results:
- PS-MPs and PS-NPs exposure led to testicular histopathological damage, including dilated seminiferous tubules and disorganized spermatocytes.
- Significant reductions in sperm count and motility were observed in exposed mice.
- Spermatocyte senescence was induced, evidenced by increased β-galactosidase activity and markers of DNA damage and cell cycle arrest.
- Activation of the PI3K/AKT/mTOR signaling pathway was associated with PS-MP and PS-NP exposure.
Conclusions:
- PS-MPs and PS-NPs induce structural damage and impair spermatogenesis in male mice.
- Spermatocyte senescence, mediated by the PI3K/AKT/mTOR pathway, is a key mechanism underlying this reproductive toxicity.
- These findings highlight the potential reproductive risks of microplastic and nanoplastic exposure in males.
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