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Transplacental and lactational transfer of polystyrene nanoplastics leads to long-term ovarian impairment in rat offspring
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Researchers found that polystyrene nanoplastics crossed the placental barrier in rats and accumulated in fetal and postnatal ovaries, causing dose-dependent damage to follicle development and ovarian structure. Exposed offspring showed reduced primordial follicle numbers, granulosa cell disorganization, and hormonal imbalances that persisted through postnatal day 60. The study suggests that maternal nanoplastic exposure during pregnancy and lactation may have long-lasting effects on female reproductive development.
• PS-NPs cross placenta and accumulate in fetal and postnatal ovaries. • Maternal PS-NP exposure disrupts folliculogenesis and ovarian structure. • Oxidative stress and hormonal imbalance accompany PS-NP–induced toxicity. • Ovarian damage from PS-NPs persists from gestation through postnatal stages. Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that can cross biological barriers and accumulate in the reproductive organs. This study evaluated developmental ovarian toxicity after maternal and lactational PS-NP exposure in rats on gestational day 20 (GD20) and postnatal days 30 and 60 (PD30, PD60). Pregnant Sprague–Dawley rats were administered PS-NPs at doses of 0.1, 1, or 10 mg/kg/day during gestation and lactation. At GD20, fetal ovaries from exposed dams showed a significant reduction in primordial follicle number and diameter, early granulosa cell disorganization, and a lower parenchyma-to-stroma ratio, indicating impaired folliculogenesis. By PD30 and PD60, ovarian alterations intensified in a dose-dependent manner, including granulosa layer thinning, follicular degeneration, and cortical disarray, which were most pronounced in the high-dose group. Fluorescence microscopy confirmed the transplacental and lactational transfer of rhodamine-labeled PS-NPs, with persistent and dose-dependent accumulation in the follicles and stroma. Biochemically, PS-NP exposure increased the total oxidant status (TOS) and oxidative stress index (OSI) while decreasing the total antioxidant capacity (TAC). Serum estradiol and progesterone levels declined markedly, consistent with oxidative and endocrine disruption. Immunohistochemistry revealed the upregulation of P53 and downregulation of BCL-2, indicating apoptosis-mediated ovarian injury. These findings demonstrate that combined gestational and lactational PS-NP exposure causes persistent, dose-dependent ovarian damage from the fetal stage through postnatal development, highlighting the reproductive risks associated with maternal nanoplastic exposure in an increasingly polluted environment.
More Papers Like This
Lactational exposure to polystyrene nanoplastics is associated with dose-related ovarian alterations in rat offspring
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In a rat study, baby females exposed to nanoplastics through their mother's milk showed smaller ovaries, fewer developing egg follicles, hormone imbalances, and more cell damage as they grew up—and the effects got worse with higher doses. This suggests that the period of breastfeeding may be a particularly vulnerable time for nanoplastic exposure to affect reproductive development, raising concerns about how these tiny plastic particles—already found in breast milk—might impact fertility later in life. More research is needed to confirm whether these effects occur in humans.
Effects of polystyrene nanoplastics on the female reproductive system in mice: Implications for ovarian function and follicular development
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Researchers exposed female mice to polystyrene nanoplastics orally for 29 days and examined the effects on their reproductive systems. They found that nanoplastic exposure disrupted estrous cycles, impaired follicle development, and altered hormone levels in a dose-dependent manner. The study suggests that nanoplastics, due to their extremely small size, may cross biological barriers and accumulate in reproductive tissues, raising concerns about potential effects on fertility.
Maternal exposure to polystyrene nanoplastics leads to ovotoxicity in female mouse offspring
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Researchers exposed pregnant mice to polystyrene nanoplastics throughout mating, pregnancy, and nursing, then examined the ovaries of their female offspring. They found that maternal nanoplastic exposure significantly reduced ovarian weight and follicle numbers in the offspring and lowered the expression of key antioxidant genes. The study suggests that nanoplastic exposure during pregnancy may pose risks to the reproductive development of female offspring.
Intergenerational and transgenerational reproductive toxicity of polystyrene microplastics in female mice
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Female mice were exposed to polystyrene microplastics during lactation and researchers tracked reproductive outcomes in both exposed mothers and their offspring through multiple generations, finding that even at doses comparable to human infant bottle-feeding exposure, microplastics induced ovarian damage and reduced fertility that persisted across generations.
Maternal exposure to polystyrene nanoplastics during gestation and lactation caused fertility decline in female mouse offspring
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When pregnant mice were exposed to nanoplastics during pregnancy and nursing, their female offspring had significantly reduced fertility as adults. The nanoplastics caused premature activation of egg cells in the ovaries and damaged crucial connections between eggs and their supporting cells. This raises concerns that a mother's exposure to nanoplastics could have lasting effects on her daughters' ability to have children.
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