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Gestational and lactational exposure to phthalates and nanoplastics induces inflammation and oxidative imbalance in the prostate of adult rats
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When pregnant rats were exposed to phthalates (chemicals found in plastics) and nanoplastics, their male offspring showed lasting inflammation, oxidative damage, and hormone-related changes in their prostate glands, even as adults. This suggests that plastic exposure during pregnancy and early life could have long-term effects on prostate health in the next generation, raising concerns about how everyday plastic chemicals might impact human development before birth.
The intrauterine microenvironment is highly susceptible to environmental disturbances, which may result in persistent effects on offspring health. Given that plastic-derived contaminants can cross the placental barrier and act as endocrine-disrupting chemicals, this study evaluated the effects of perinatal exposure to an environmentally relevant phthalate mixture (PM) and nanoplastics (NPs) on the prostate of adult rats. Pregnant Sprague-Dawley rats were allocated into 6 experimental groups: Ctrl (vehicle), T1 (20 μg/kg/d PM), T2 (200 mg/kg/d PM), T3 (NPs: 1.0 mg/kg/d), T4 (20 μg PM + NPs), and T5 (200 mg PM + NPs). Treatments were administered orally from gestational day 10 to postnatal day (PND) 21. Male offspring were euthanized on PND120, and ventral prostate samples were collected. Histological evaluation revealed increased inflammatory foci and stromal expansion in all exposed groups (T1-T5), along with reduced luminal compartment in T1, T3, and T4 compared with controls. All treated groups showed increased total and degranulated mast cells and enhanced androgen receptor immunoreactivity. Tumor necrosis factor (Tnf) expression was increased in all exposure groups, whereas Rela gene expression was elevated in the T4 and T5 groups. Oxidative stress analysis demonstrated increased lipid peroxidation and glutathione S-transferase (GST) activity in all treated animals. Catalase (CAT) activity was reduced in T1, T3, and T5, whereas superoxide dismutase (SOD) activity increased in T3, T4, and T5. Elevated levels of reduced, oxidized, and total glutathione (GSH, GSSG, tGSH) were observed in T5. Overall, perinatal exposure to PM and NPs induced persistent inflammation and altered redox status in the prostate, increasing susceptibility to pathological disorders.
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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.
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.
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.
Perinatal exposure to polystyrene microplastics induces multigenerational impairment of male reproduction via disrupted steroidogenesis and proteostasis
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Scientists found that when pregnant and nursing rats were exposed to tiny plastic particles (microplastics), their male babies and grandbabies had damaged reproductive systems with lower sperm counts and reduced fertility hormones. While the grandbabies showed some ability to recover from this damage, the study suggests that microplastics in our environment could potentially harm male fertility across multiple generations. This research is concerning because humans are increasingly exposed to microplastics through food, water, and air.
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.
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