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Polystyrene microplastics disrupt the blood-testis barrier integrity through ROS-Mediated imbalance of mTORC1 and mTORC2
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Researchers found that polystyrene microplastics can disrupt the blood-testis barrier in mice by triggering oxidative stress and disrupting cellular signaling pathways. The damage was linked to an imbalance between two protein complexes that regulate cell structure and barrier integrity in reproductive tissues. The study suggests that microplastic exposure may impair male reproductive health by compromising the protective barrier that shields developing sperm cells.
It has been found that polystyrene microplastics (PS-MPs) exposure leads to decreased sperm quality and quantity, and we aim to explore the underlying mechanisms. Therefore, we gave 20 mg/kg body weight (bw) and 40 mg/kg bw 4 μm and 10 μm PS-MPs to male Balb/c mice by gavage. RNA sequencing of testes was performed. After PS-MPs exposure, blood-testis barrier (BTB) integrity was impaired. Since cytoskeleton was closely related to BTB integrity maintenance, and cytoskeleton disorganization could be induced by PS-MPs exposure in the testis, which resulted in the truncation of actin filaments and disruption of BTB integrity. Such processes were attributed to the differential expression of Arp3 and Eps8 (two of the most important actin-binding proteins). According to the transcriptome sequencing results, we examined the oxidative stress level in the testes and Sertoli cells. We found that PS-MPs exposure induced increased reactive oxygen species (ROS) level, which destroyed the balance between mTORC1 and mTORC2 (the mTORC1 activity was increased, while the mTORC2 activity was decreased). In conclusion, PS-MPs induced the imbalance of mTORC1 and mTORC2 via the ROS burst, and altered the expression profile of actin-binding proteins, resulting in F-actin disorganization and reduced expression of junctional proteins in the BTB. Eventually PS-MPs led to BTB integrity disruption and spermatogenesis dysfunction.
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Polystyrene microplastics induce blood–testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats
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Researchers fed rats polystyrene microplastics for 90 days and found significant damage to male reproductive health, including reduced sperm quality, damaged sperm-producing tissue, and increased cell death. The study identified a specific molecular pathway where microplastics triggered oxidative stress that disrupted the blood-testis barrier, a critical protective structure in the testes. These findings provide new evidence that microplastic exposure may pose risks to male reproductive function.
Adverse effects and potential mechanisms of polystyrene microplastics (PS-MPs) on the blood-testis barrier
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This review examines how polystyrene microplastics damage the blood-testis barrier, a critical structure that protects developing sperm cells from harmful substances. Microplastics can break down this barrier through oxidative stress, inflammation, and disruption of gut bacteria, allowing pollutants and immune cells to enter the reproductive system. These findings suggest that microplastic exposure may contribute to declining male fertility, a trend observed globally in recent decades.
Polystyrene microplastic exposure in mice: oxidative stress-induced testicular damage, AR gene suppression, and histopathological alterations
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Researchers exposed mice to polystyrene microplastics at two different concentrations and observed significant impacts on reproductive health, including increased oxidative stress in testicular tissue. The study found elevated reactive oxygen species, reduced sperm count and motility, and suppression of androgen receptor gene expression. Evidence indicates that microplastic exposure may pose reproductive health risks by disrupting antioxidant defenses and damaging testicular cells.
Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis
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Researchers found that polystyrene nanoplastics worsened reproductive damage in male mice already fed a high-fat diet, reducing sperm quality and testosterone production beyond what obesity alone caused. The nanoplastics disrupted the protective blood-testis barrier and increased oxidative stress in reproductive tissues. The study suggests that nanoplastic exposure combined with obesity may create compounding risks to male fertility.
Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway
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Researchers exposed mice to polystyrene microplastics for 35 days and found significant male reproductive toxicity, including decreased sperm counts and motility, increased sperm abnormalities, and reduced testosterone levels. The microplastics caused structural damage to the seminiferous tubules and triggered endoplasmic reticulum stress in testicular tissue. The study suggests that microplastic exposure may impair male reproductive health through stress-related signaling pathways in the testes.
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