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Polyethylene Nanoplastic Exposure Causes Miscarriage by Impairing Trophoblast NAD + Metabolism via Mitochondrial Dysfunction
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Scientists found tiny plastic particles (from everyday polyethylene, used in bags and packaging) in placental tissue from every pregnancy sample they studied, and higher levels were linked to increased miscarriage risk. In mice and lab-grown placental cells, these plastic particles damaged the cell's energy-producing mitochondria, which blocked processes needed for a healthy pregnancy to take hold, but treatments that protected mitochondria or restored key molecules reversed the damage. This research suggests everyday plastic exposure may pose a real risk to pregnancy, while also pointing to possible ways to protect against
ABSTRACT Micro‐ and nanoplastics (MNPs) are emerging environmental pollutants of global concern, yet their reproductive toxicity and underlying mechanisms remain poorly understood. Here, we identify villous accumulation of polyethylene (PE) as a potential risk factor associated with miscarriage and investigate the underlying mechanisms using well‐characterized PE nanoparticles. PE fragments were detected in all examined human villous tissues and higher levels of these fragments showed a positive association with miscarriage risk (OR = 1.13, 95% CI, 1.00–1.28). In mice, oral exposure to PE‐MNPs led to dose‐dependent embryo resorption. In trophoblasts, PE nanoplastics (PE‐NPs) were efficiently internalized and subsequently impaired cell migration and invasion. Mechanistically, PE‐NPs accumulated within mitochondria, causing structural damage, downregulation of nicotinamide phosphoribosyltransferase (NAMPT), and depletion of nicotinamide adenine dinucleotide (NAD + ), which in turn suppressed fibroblast growth factor 2 (FGF2) expression, resulting in impaired trophoblast migration and invasion. Supplementation with mitochondria‐protective peptide, NAD + or FGF2 attenuated trophoblast dysfunction and reduced embryo resorption. These findings provide mechanistic insight into PE‐NPs‐induced reproductive toxicity and suggest a potential therapeutic target to mitigate the impact of NPs exposure on maternal‐fetal health.
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Cellular uptake of micro and nano plastics Induces Mitochondrial Dysfunction
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Scientists found that tiny plastic particles from our environment can travel through the bloodstream and get absorbed into placenta cells, where they damage the cell's energy-producing "batteries" (mitochondria) and cause inflammation. In mouse and lab-based human cell studies, this damage weakened the cells' ability to function properly, raising concerns that microplastic exposure during pregnancy could potentially harm placental health and fetal development. More research is needed to confirm these effects in humans, but the findings suggest another reason to minimize plastic exposure during pregnancy.
Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage
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In mouse and cell studies, polystyrene nanoplastics at doses near real-world human exposure levels caused miscarriage by blocking the movement of placental cells needed for a healthy pregnancy. The nanoplastics triggered a cellular recycling process called autophagy that broke down key proteins required for placental cell migration and invasion.
Intracellular fate of micro- and nanoplastics in human placenta: Organelle-specific toxicity and mechanistic convergence
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Scientists have found tiny plastic particles (microplastics and nanoplastics) inside the placenta, and this review pulls together existing research to explain what might be happening at a cellular level: these particles seem to overwhelm cells' waste-disposal systems, damage their energy-producing mitochondria, and trigger stress responses that don't fully shut off. This matters because the placenta is what nourishes and protects a developing baby, so if plastics are disrupting its cells this way, it could have implications for fetal development, though this is a proposed theoretical model based on current evidence, not a confirmed cause-and-effect finding, and more
Exposure to high dose of polystyrene nanoplastics causes trophoblast cell apoptosis and induces miscarriage
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Exposure to polystyrene nanoplastics triggered a cell death pathway in the placental cells (trophoblasts) that are essential for maintaining pregnancy, leading to miscarriage in mice. This finding raises concerns that nanoplastic exposure during pregnancy could harm fetal development by damaging the critical cells that connect mother and baby.
Environmentally relevant polyethylene terephthalate (PET) microplastics induce functional and oxidative alterations in sheep placental cells In vitro
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Scientists exposed sheep placenta cells to tiny plastic particles (from PET, the plastic used in water bottles) at levels animals might realistically encounter from eating contaminated feed. The smallest plastic bits, less than 20 microns, thinner than a human hair, damaged the cells' energy production, increased cell death, and impaired their normal function, even at very low doses. While this study was done in sheep, it raises concern about how the microplastics we all encounter daily might similarly affect the placenta during human pregnancy, a critical organ for supporting a developing baby.
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