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The Potential Mechanisms Involved in the Disruption of Spermatogenesis in Mice by Nanoplastics and Microplastics
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Researchers examined how polystyrene nanoplastics and microplastics disrupt spermatogenesis in mice through different molecular mechanisms. The study found that nanoplastics primarily affected retinoic acid metabolism, while microplastics influenced pyruvate and thyroid hormone metabolism, suggesting that particle size determines distinct pathways of reproductive harm in male mammals.
PS-NPs were predominantly involved in regulating retinoic acid metabolism, whereas PS-MPs primarily influenced pyruvate metabolism and thyroid hormone metabolism. Our results highlight the different molecular mechanisms of PS-NPs and PS-MPs in the impairment of spermatogenesis in male mammals for the first time, providing valuable insights into the precise mechanisms of PS-NPs and PS-MPs in male reproduction.
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Reproductive Toxicity of Chronic Exposure To Polystyrene Microplastics And The Molecular Mechanism of Decrease In Testosterone Levels In Male Mice
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Chronic exposure to polystyrene microplastics lowered testosterone levels in male mice and disrupted reproductive organ function. The study identified molecular pathways through which microplastics interfere with male hormone production, with implications for reproductive health in humans exposed through diet.
Toxicity to the Male Reproductive System after Exposure to Polystyrene Nanoplastics: A Macrogenomic and Metabolomic Analysis
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Researchers exposed male mice to polystyrene nanoplastics of different sizes through their drinking water for four months and found significant harm to reproductive function. The nanoplastics disrupted gene activity and metabolic pathways in the gut, which was linked to reduced sperm quality and testicular damage. The study suggests that long-term nanoplastic exposure through drinking water may pose risks to male reproductive health.
Polystyrene microplastics induced male reproductive toxicity in mice
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Researchers exposed male mice to polystyrene microplastics of different sizes and found that the particles accumulated in testicular tissue and entered reproductive cells. After 28 days of exposure, sperm quality and testosterone levels declined, and tissue examination revealed disorganized sperm-producing cells and inflammation. The study suggests that microplastic exposure may pose risks to male reproductive health in mammals.
The emerging risk of exposure to nano(micro)plastics on endocrine disturbance and reproductive toxicity: From a hypothetical scenario to a global public health challenge
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Researchers administered polystyrene nanoplastics orally to male rats for five weeks and found significant reductions in testosterone, LH, and FSH levels, sperm DNA damage, altered testicular gene expression, and dose-dependent histological lesions, indicating that nanoplastic exposure disrupts the hormonal axis governing male reproductive function.
In Vitro Nano-Polystyrene Toxicity: Metabolic Dysfunctions and Cytoprotective Responses of Human Spermatozoa
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Researchers investigated the effects of polystyrene nanoplastics (50 and 100 nm) on mature human sperm cell metabolism in vitro. The study found that smaller 50 nm particles showed higher toxicity, causing acrosomal damage, oxidative stress, DNA fragmentation, and decreased mitochondrial activity, while 100 nm particles primarily affected the acrosome, suggesting size-dependent impacts of nanoplastics on reproductive cell function.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.