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Maternal exposure to nanopolystyrene induces neurotoxicity in offspring through P53-mediated ferritinophagy and ferroptosis in the rat hippocampus
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When pregnant and nursing rats were fed nanoplastics, their offspring showed impaired learning and memory due to a specific type of cell death called ferroptosis in the brain's hippocampus. The nanoplastics triggered a chain reaction involving oxidative stress and iron buildup that damaged developing brain cells, suggesting that maternal exposure to nanoplastics during pregnancy and breastfeeding could harm offspring brain development.
There are increasing concerns regarding the rapid expansion of polystyrene nanoplastics (PS-NPs), which could impact human health. Previous studies have shown that nanoplastics can be transferred from mothers to offspring through the placenta and breast milk, resulting in cognitive deficits in offspring. However, the neurotoxic effects of maternal exposure on offspring and its mechanisms remain unclear. In this study, PS-NPs (50 nm) were gavaged to female rats throughout gestation and lactation to establish an offspring exposure model to study the neurotoxicity and behavioral changes caused by PS-NPs on offspring. Neonatal rat hippocampal neuronal cells were used to investigate the pathways through which NPs induce neurodevelopmental toxicity in offspring rats, using iron inhibitors, autophagy inhibitors, reactive oxygen species (ROS) scroungers, P53 inhibitors, and NCOA4 inhibitors. We found that low PS-NPs dosages can cause ferroptosis in the hippocampus of the offspring, resulting in a decline in the cognitive, learning, and memory abilities of the offspring. PS-NPs induced NOCA4-mediated ferritinophagy and promoted ferroptosis by inciting ROS production to activate P53-mediated ferritinophagy. Furthermore, the levels of the antioxidant factors glutathione peroxidase 4 (GPX4) and glutathione (GSH), responsible for ferroptosis, were reduced. In summary, this study revealed that consumption of PS-NPs during gestation and lactation can cause ferroptosis and damage the hippocampus of offspring. Our results can serve as a basis for further research into the neurodevelopmental effects of nanoplastics in offspring.
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Researchers exposed pregnant rats to nanoplastics and then analyzed protein expression in the hippocampus of their offspring. They found reduced levels of proteins important for neural development and increased levels of inhibitory proteins, with pathway analysis highlighting ferroptosis as a key mechanism. The study suggests that prenatal nanoplastic exposure may contribute to cognitive deficits in offspring by disrupting brain protein expression during development.
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Researchers showed that polystyrene nanoplastics impair spatial memory in mice by triggering a cascade in which hippocampal oxidative stress activates microglia to release extracellular traps, sustaining neuroinflammation that drives neuronal ferroptosis — a form of iron-dependent cell death — and that the antioxidant N-acetylcysteine blocks this entire pathway and preserves cognitive function.
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Adult female zebrafish were exposed to polystyrene nanoplastics for 28 days. The particles passed to their embryos and larvae, which had lower hatching rates, more malformations, reduced movement and fewer neurons in part of the brain. The damage was driven by oxidative stress and two cell-death pathways, and antioxidant treatment partly reversed it.
Maternal exposure to polystyrene nanoplastics causes brain abnormalities in progeny
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Researchers found that maternal exposure to polystyrene nanoplastics caused brain abnormalities in offspring, demonstrating that nanoplastics can cross maternal barriers and affect neurological development in progeny with implications for developmental toxicology.
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.
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