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Oral exposure to polystyrene nanoplastics altered the hypothalamic–pituitary–testicular axis role in hormonal regulation, inducing reproductive toxicity in albino rats
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This study found that oral exposure to polystyrene nanoplastics disrupted the hormone signaling pathway between the brain and testes in male rats, leading to reproductive damage. The nanoplastics interfered with the hormones that regulate sperm production and testicular function. These findings add to growing evidence that nanoplastic exposure through food and water could be a contributing factor to declining male fertility.
Altogether, the current findings provide novel perspectives on PS-NP general toxicity with specific reference to male reproductive toxicity.
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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.
Adolescent exposure to polystyrene nanoplastics induces male reproductive damage via the microbiome-gut-testis axis
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Researchers exposed adolescent rats to polystyrene nanoplastics for five weeks and observed dose-dependent damage to testicular tissue, disrupted spermatogenesis, and compromised blood-testis barrier integrity. The study revealed a novel microbiome-gut-testis axis mechanism, where nanoplastics altered gut bacteria composition, which in turn contributed to reproductive toxicity in developing males.
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.
Oral exposure to polystyrene nanoplastics reduced male fertility and even caused male infertility by inducing testicular and sperm toxicities in mice
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Researchers fed male mice polystyrene nanoplastics of different sizes (25, 50, and 100 nm) for 56 days and found that all sizes reduced fertility and some caused complete infertility. The nanoplastics accumulated in the testes, causing oxidative stress, cell death, and inflammation that damaged sperm and reproductive tissue. This study raises concerns that human exposure to nanoplastics through food and water could contribute to declining male fertility.
Lactational exposure to polystyrene nanoplastics induces oxidative stress, testicular histological alterations, and impaired sperm quality in rat offspring
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In rats, mothers exposed to nanoplastics during breastfeeding passed on effects that damaged their male offspring's developing testicles, lowering sperm count, motility, and quality while disrupting reproductive hormones. Though this is animal research, it raises concerns that nanoplastics in breast milk could harm reproductive development in human infants, an area that needs more study.
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