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Polystyrene nanoparticles induced adverse pregnancy outcomes via the activation of placental ferroptosis and gut microbiota dysfunction
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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.
Maternal exposure to microplastics, particularly polystyrene nanoparticles (PS-NPs), is an emerging environmental threat associated with adverse pregnancy outcomes. However, the underlying mechanisms, especially the potential involvement of placental ferroptosis and gut microbiota, remain largely unexplored. This study aimed to elucidate whether and how maternal exposure to 50-nm PS-NPs disrupts pregnancy in a mouse model, with a focus on gut microbiota dysbiosis and placental ferroptosis. We found that PS-NPs exposure during pre-mating and gestation induced gut microbiota dysbiosis (e.g., increased Campylobacterota and Helicobacter) and triggered placental ferroptosis, as evidenced by iron accumulation, lipid peroxidation, and dysregulation of key proteins associated with ferroptosis. These cellular disruptions led to impaired placental barrier function, increased inflammation, and ultimately, adverse pregnancy outcomes, including elevated embryo resorption and reduced fetal weight. Crucially, correlation analysis linked specific gut microbiota alterations to ferroptosis and pregnancy loss. Furthermore, in vitro experiments confirmed that ferroptosis inhibitors alleviated PS-NPs-induced trophoblast dysfunction. These results suggest that maternal exposure to PS‑NPs may contribute to adverse pregnancy outcomes via inducing gut‑microbiota dysbiosis and placental ferroptosis, which might be potential focus for future mechanistic and therapeutic investigations.
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Polystyrene Nanoplastics induced placental toxicology by activating Keap1-mediated ferroptosis via METTL3-dependent m6A methylation
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Scientists found that tiny plastic particles called nanoplastics can damage the placenta during pregnancy by triggering a harmful process called ferroptosis, which kills cells through iron buildup. The study used lab cells and pregnant mice to show how these plastic particles disrupt the body's natural protective systems in placental tissue. This research helps explain why microplastics in our environment might pose risks during pregnancy, though more studies are needed to understand the full impact on human health.
Polystyrene nanoplastics impair placental function and promote embryo resorption through ROS-mediated ferroptosis-related injury.
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In a study on pregnant mice and human placental cells, tiny plastic particles called nanoplastics (the kind that break down from everyday plastic waste) crossed the placenta, damaged its cells, and triggered a harmful type of cell death caused by oxidative stress—ultimately leading to more pregnancy loss in the mice. While this research was done in animals and lab-grown cells rather than in humans, it raises real concerns about how the microplastics we're increasingly exposed to might affect pregnancy health, and points to specific biological pathways that future treatments or protective strategies could target.
Gut microbiota contributes to polystyrene nanoplastics-induced fetal growth restriction by disturbing placental nicotinamide metabolism
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Researchers found that pregnant mice exposed to polystyrene nanoplastics experienced placental damage and metabolic disruptions that restricted fetal growth. The nanoplastics altered the mothers' gut bacteria, which in turn disturbed nicotinamide metabolism in the placenta, a key pathway for fetal development. The study suggests that nanoplastic exposure during pregnancy may harm offspring development through indirect effects on the gut-placenta connection.
Gestational exposure to nanoplastics disrupts fetal development by promoting the placental aging via ferroptosis of syncytiotrophoblast
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This mouse study found that exposure to nanoplastics during pregnancy caused placental aging and fetal growth restriction through a process called ferroptosis -- a type of iron-dependent cell death -- in the cells that form the barrier between mother and baby. When researchers blocked the ferroptosis process, fetal weight improved, suggesting this pathway could be a target for protecting pregnancies from nanoplastic-related harm.
Maternal exposure to polystyrene nanoparticles retarded fetal growth and triggered metabolic disorders of placenta and fetus in mice
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Researchers exposed pregnant mice to polystyrene nanoplastics through drinking water and found that higher concentrations led to significantly reduced fetal weight. The nanoplastics caused abnormal cell structures in the placenta and disrupted metabolic processes in both placental tissue and fetal livers. The study suggests that maternal nanoplastic exposure during pregnancy can cross the placental barrier and interfere with normal fetal growth and metabolism.
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