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Polyethylene terephthalate (PET) microplastics induced male reproductive toxicity in mice by activating the p38-MAPK
Xin Zhang1, Tianyi Ma2, Jingran Sun2
1Baotou Teachers' College, School of Ecological Environment, Baotou 014000, China; Military Medical Sciences Academy, Academy of Military Sciences, Tianjin 300050, China.
Abstract:
Microplastics are widespread environmental pollutants that can easily enter the bodies of living organisms through various means, arousing extensive concern. However, research regarding the influence of polyethylene terephthalate microplastics (PET-MPs) on the mammalian reproductive system is limited. This study explored the mechanisms by which PET-MPs induce reproductive toxicity in male mice. The results showed that after 90 days of continuous gavage exposure, PET-MPs with sizes of 50, 200, and 1000 nm accumulated in the testicular tissue. The results of the experiment showed the sperm quality and related hormone levels of mice declined. Hematoxylin and eosin (H&E) staining showed that spermatogenic cells were shed, disordered in arrangement, and vacuolated. Immunohistochemical results showed that spermatogenic cell proliferation was inhibited, and apoptosis was significantly increased. Transcriptome sequencing showed that PET-MP exposure activated the MAPK pathway in testicular tissues. Through the detection of key genes, proteins, and inflammatory factor levels in this pathway, we demonstrated that PET-MP exposure elevated inflammatory factor levels. These results provide a theoretical foundation for elucidating the impact of PET-MP exposure on the mammalian reproductive system.
Insights
Polyethylene terephthalate microplastics (PET-MPs) accumulate in male mouse testes, impairing sperm quality and hormone levels. PET-MP exposure triggers inflammation and cell death, impacting male reproductive health.
Area of Science:
- Environmental Science
- Toxicology
- Reproductive Biology
Background:
- Microplastics are pervasive environmental pollutants with increasing human exposure.
- Research on the specific effects of polyethylene terephthalate microplastics (PET-MPs) on mammalian reproductive systems is limited.
- Understanding the reproductive toxicity mechanisms of PET-MPs is crucial for public health.
Purpose of the Study:
- To investigate the impact of PET-MPs on male mouse reproductive toxicity.
- To elucidate the underlying mechanisms of PET-MP-induced reproductive damage.
- To assess the effects of PET-MPs on testicular tissue, sperm quality, hormone levels, and cellular pathways.
Main Methods:
- Male mice were exposed to varying sizes of PET-MPs (50, 200, 1000 nm) via continuous gavage for 90 days.
- Testicular tissue accumulation, sperm quality, and hormone levels were analyzed.
- Histopathological examination using Hematoxylin and eosin (H&E) staining was performed.
- Immunohistochemistry was used to assess cell proliferation and apoptosis.
- Transcriptome sequencing identified activated pathways, followed by analysis of key genes, proteins, and inflammatory factors.
Main Results:
- PET-MPs were found to accumulate in testicular tissue.
- Sperm quality and male hormone levels significantly declined post-exposure.
- Histopathology revealed spermatogenic cell shedding, disordered arrangement, and vacuolation.
- PET-MP exposure inhibited spermatogenic cell proliferation and increased apoptosis.
- Transcriptome analysis indicated activation of the MAPK pathway, with elevated inflammatory factors.
Conclusions:
- PET-MPs induce reproductive toxicity in male mice.
- The mechanism involves testicular accumulation, impaired spermatogenesis, hormonal imbalance, and inflammation via the MAPK pathway.
- These findings highlight the potential reproductive risks associated with PET-MP environmental exposure.
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