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Polyethylene terephthalate (PET) microplastics induced male reproductive toxicity in mice by activating the p38-MAPK pathway
Summary
Researchers exposed male mice to PET microplastics of various sizes for 90 days and found that the particles accumulated in testicular tissue. The microplastics reduced sperm quality, damaged testicular structure, and triggered cell death through a specific stress-response pathway called p38-MAPK. The study suggests that PET microplastic exposure may pose risks to male reproductive health through oxidative stress and programmed cell death.
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.
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