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Prenatal microplastic exposure-induced testicular developmental toxicity and its long-term hazards in male rat offspring.
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Pregnant rats were given microplastics during pregnancy, and their male offspring had lower birth weights, smaller testicles, reduced testosterone and luteinizing hormone levels, fewer hormone-producing Leydig cells, and changes in sperm, effects that persisted from birth into adulthood.
The pervasive environmental presence of microplastics (MPs) raises concerns regarding their potential impacts on reproductive health, particularly in the context of prenatal exposure. This study aimed to establish a polystyrene microplastics (PS-MPs) exposure model in pregnant rats and to investigate the subsequent effects on the growth, hormonal profiles, steroidogenic enzyme expression, and testicular histology of male offspring from birth to adulthood. Pregnant rats were administered PS-MPs at doses of 1 mg/kg/day (MPs-L) and 10 mg/kg/day (MPs-H) during gestational days 10-20. Results indicated that birth weights in the MPs-L and MPs-H groups decreased to 88.7% and 85.3% of controls, respectively, with persistent intrauterine growth restriction and no catch-up growth observed. Testicular morphology analysis revealed significant reductions in testicular area and diameter in neonatal rats, alongside adult testicular index decline and altered sperm parameters. Hormonal assessments showed concentration-dependent decreases in serum testosterone levels during neonatal and adult stages, coupled with reduced luteinizing hormone levels in adults, indicating a non-classical "low testosterone-low luteinizing hormone" phenotype. Molecular evaluations demonstrated selective suppression of key steroidogenic genes (Star and 3β-Hsd) in neonatal and adult testicular tissues, while Leydig cell counts were significantly diminished. In conclusion, prenatal exposure to MPs had long-lasting repercussions on Leydig cell functionality and the spermatogenic environment, leading to dual structural and endocrine impairments that may have critical implications for male reproductive health. Future studies should further explore the mechanisms underpinning these effects and potential interventions.
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Developmental Effects of Intrauterine and Lactational Exposure to Nanoplastics and Phthalates on Rat Testis
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A new study found that when pregnant rats were exposed to nanoplastics and phthalates (chemicals found in plastics), their male offspring showed lasting damage to testicle development, including changes to sperm-producing cells and increased oxidative stress that persisted into adulthood. The combination of both chemicals caused more harm than either one alone, suggesting that real-world exposure to multiple plastic-related pollutants during pregnancy could pose bigger risks to male reproductive health than scientists previously realized—though more research is needed to confirm these effects translate to humans.
Dose-Dependent Effect of Polystyrene Microplastics on the Testicular Tissues of the Male Sprague Dawley Rats
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Male rats exposed to increasing doses of polystyrene microplastics showed dose-dependent testicular damage including disrupted spermatogenesis and altered hormone levels, suggesting potential reproductive toxicity from microplastic accumulation.
Prenatal and postnatal exposure to polystyrene microplastics induces testis developmental disorder and affects male fertility in mice
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Researchers exposed pregnant mice and their offspring to polystyrene microplastics from gestation through early life and found significant disruption to testicular development and male reproductive function. The exposed males showed reduced sperm quality, lower testosterone levels, and structural damage to testicular tissue. The study suggests that early-life microplastic exposure may have lasting effects on male fertility.
Prenatal exposure to polystyrene nanoplastics caused testicular development toxicities and relative mechanisms in male offspring mice from embryo to adulthood
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Scientists exposed pregnant mice to nanoplastics (tiny plastic particles found in our environment, blood, and even placentas) and found their male offspring had slowed growth before birth, hit puberty earlier, and had reduced fertility as adults. The nanoplastics appeared to disrupt key genes and cells needed for normal testicle development and hormone production. While this is animal research, it adds to growing evidence that plastic exposure during pregnancy could affect a baby's reproductive development later in life.
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