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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.
Micro(nano)plastics (MNPs), are emerging environmental pollutants that have garnered widespread attention. Epidemiological and animal studies have shown that MNPs exposure during pregnancy is associated with adverse pregnancy outcomes, such as intrauterine growth restriction (IUGR) and miscarriage. However, the underlying mechanisms remain poorly understood. In this study, we found that exposure to a high dose (1 μg·mL-1) of 100 nm polystyrene nanoparticles (NPs) from gestational day (GD) 0 to GD17 significantly decreased fetal weight and increased the number of resorptions compared to the control group. Moreover, fetal weight was significantly lower in the high-dose group than in the low-dose (0.1 μg·mL-1) group. Meanwhile, ferroptosis and senescence were observed in placentas from mice exposed to high dose of NPs. In vitro experiments using human syncytiotrophoblast (STB) cells differentiated from BeWo cells, we found that NPs caused ferroptosis and senescence in STB cells. Subsequent investigations revealed that the inhibition of the ferroptosis signaling by ferrostain-1 (Fer-1) or deferiprone (DFP) ameliorated senescence induced by NPs in human STB cells. Furthermore, alleviating placental senescence using Fer-1 significantly improves fetal weight loss caused by NPs exposure during pregnancy in mice. Taken together, our results demonstrated that NPs exposure during pregnancy activated the ferroptosis pathway in placental STB, resulting in senescence of STB, which may attribute to the NPs-induced IUGR. This study not only elucidated the mechanistic link between NPs exposure and adverse pregnancy outcomes but also highlighted the necessity for targeted interventions to protect fetal health, underscoring the broader implications for environmental and public health policy.
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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.
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.
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 induce fetal growth restriction via a novel NMNAT3 depletion cascade disrupting placental mitochondrial energetics and activating ferritinophagic ferroptosis
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Exposure to polystyrene nanoplastics during pregnancy disrupted nicotinamide metabolism in the placenta, depleted NAD and triggered ferroptosis, a form of cell death, which restricted fetal growth. Giving nicotinamide inhibited ferroptosis and improved pregnancy outcomes. The abstract does not name the animal studied.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
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Researchers found that polystyrene nanoplastics disrupt the blood-brain barrier in mice by triggering ferroptosis — an iron-dependent form of cell death — in brain microvascular endothelial cells, and that blocking ferroptosis with a targeted drug reduced tight junction protein loss and restored barrier integrity.
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