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Prepregnancy Exposure to High Doses of Nanoplastics Triggers Persistent Vaginal Microbiome Dysbiosis to Induce Adverse Pregnant Outcomes
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In mice, exposure to high doses of nanoplastics before pregnancy disrupted the vaginal microbiome, causing lasting inflammation and nutrient depletion that led to miscarriage and poor embryo growth, even after the plastic particles were gone. Treatments like nutrient supplements or anti-inflammatory drugs reversed the damage, suggesting nanoplastic pollution could threaten fertility and pregnancy health, though more research is needed to confirm this in humans.
Abstract The global accumulation of nanoplastics poses wide concerns for human health. Although their toxicity in various organs is being uncovered, their impact on vaginal microbiomes that are essential for healthy reproduction remains largely unknown. Here, we discover a previously unrecognized long-term nanoplastic reproductive toxicity that prepregnant exposure to high doses of aged polystyrene nanoparticles (aPS-NPs) induces mouse miscarriage and restricts embryo development by persistently causing vaginal microbial dysbiosis (an increase in Aerococcus urinae abundance), vaginal glutamine depletion (suppression of Slc1a5-mediated import of glutamine from outside cells to intracells), and vaginal inflammation (up-regulation of Ifnar1, Il-1β, and Il-18) from prepregnancy to pregnancy, despite the fact that aPS-NPs are almost undetectable in the vagina on D14 in pregnancy. Transplant of A. urinae into the vaginal tract exacerbates these processes and adverse pregnancy outcomes. Interventions, such as Slc1a5 overexpression, glutamine supplement, or anti-inflammatory treatment, can effectively recover these processes and alleviate the adverse outcomes. Therefore, this study not only demonstrates a previously unrecognized long-term nanoplastic reproductive toxicity by persistently causing vaginal dysbiosis, metabolic dysfunctions, and inflammation, ultimately inducing adverse pregnant outcomes, but also provides experimental basis for targeted therapies to combat the escalating threat of nanoplastic pollution.
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Researchers found that exposing pregnant mice to micro- and nanoplastics led to increased embryo loss, reduced embryonic weight, and smaller placentas. The plastic particles impaired a critical process called syncytialization, where placental cells fuse together to form a functional barrier, by activating a stress-response signaling pathway. The study suggests that prenatal microplastic exposure could disrupt placental development and contribute to poor pregnancy outcomes.
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Researchers exposed pregnant mice to 50-nanometer polystyrene nanoparticles and found that the particles caused adverse pregnancy outcomes through two interconnected mechanisms: disruption of gut microbiota and activation of ferroptosis in placental tissue. The nanoparticle exposure altered the composition of beneficial gut bacteria and triggered iron-dependent cell death in the placenta. The study suggests that maternal exposure to nanoplastics during pregnancy may threaten reproductive health through gut-placenta axis disruption.
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