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Effects of exposure to nano-plastic drinking during pregnancy on cognitive related proteins in offspring of SD rats
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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.
Nanoplastics, an emerging contaminant, pose risks to fetal neural development, transferring from mother to offspring via placenta and breast milk. Assessing these risks, hippocampal CA3 samples from nanopolystyrene-exposed rat offspring were proteomically analyzed. Findings revealed reduced expression of neural developmental proteins (KIF21A, STMN2, DMTN, DLG1) and increased inhibitory proteins (PZP, α-2M, FN1, SERPINA1, ALOX15) in the hippocampus. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted ferroptosis enrichment, validated by significantly expressed ALOX15 and TF proteins. These alterations suggest nanopolystyrene’s potential contribution to cognitive deficits and neurodevelopmental disorders, emphasizing its hazardous impact on neural development. This study provides novel insights into nanopolystyrene’s risks.
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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.
ROS-driven crosstalk between ferroptosis and necroptosis mediates neurotoxicity induced by maternal exposure to polystyrene nanoplastics in zebrafish
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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.
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.
Prenatal exposure on nanoplastics: A study of spatial transcriptomics in hippocampal offspring
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Using advanced spatial gene-mapping technology, researchers found that prenatal exposure to nanoplastics caused significant changes in gene activity throughout the hippocampus, the brain region responsible for learning and memory, in rat offspring. The nanoplastics altered the expression of genes involved in brain cell communication, energy production, and development. This study provides detailed evidence that nanoplastic exposure during pregnancy could disrupt brain development in ways that may affect cognitive function.
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.
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