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61,005 resultsShowing papers similar to Gestational exposure to nanoplastics disrupts fetal development by promoting the placental aging via ferroptosis of syncytiotrophoblast
ClearPolystyrene nanoparticles induced adverse pregnancy outcomes via the activation of placental ferroptosis and gut microbiota dysfunction
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
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.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
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.
Maternal exposure to nanopolystyrene induces neurotoxicity in offspring through P53-mediated ferritinophagy and ferroptosis in the rat hippocampus
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.
Gestational exposure to micro- and nanoplastics leads to poor pregnancy outcomes by impairing placental trophoblast syncytialization
Researchers found that exposing pregnant mice to micro- and nanoplastics led to increased embryo loss, reduced embryonic weight, and smaller placentas. The plastic particles impaired a critical process called syncytialization, where placental cells fuse together to form a functional barrier, by activating a stress-response signaling pathway. The study suggests that prenatal microplastic exposure could disrupt placental development and contribute to poor pregnancy outcomes.
Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Microplastic exposure induces preeclampsia-like symptoms via HIF-1α/TFRC-mediated ferroptosis in placental trophoblast cells
Researchers exposed pregnant rats to polystyrene microplastics and found that the particles induced symptoms resembling preeclampsia, including elevated blood pressure and increased protein in urine. The microplastics triggered a type of cell death called ferroptosis in placental cells by activating a specific signaling pathway that led to iron overload and oxidative damage. The study identifies microplastic-induced placental cell death as a potential mechanism linking environmental plastic exposure to pregnancy complications.
Effects of exposure to nano-plastic drinking during pregnancy on cognitive related proteins in offspring of SD rats
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.
HIF-1α/HO-1-Mediated Ferroptosis Participates in Polystyrene Nanoplastics-Induced Intergenerational Cardiotoxicity
When pregnant mice were exposed to polystyrene nanoplastics, the particles crossed into offspring hearts and caused heart damage through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics activated a specific molecular pathway involving HIF-1 alpha and HO-1 that led to iron buildup, mitochondrial injury, and oxidative stress in heart tissue. This study raises concerns that maternal nanoplastic exposure during pregnancy could harm fetal heart development in ways that may have lasting consequences.
Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation
Researchers found that polystyrene nanoplastics trigger ferroptosis — a form of iron-dependent cell death driven by fat oxidation — in pig egg cells, disrupting their maturation and reproductive viability. This finding raises concerns about nanoplastic exposure potentially impairing fertility by damaging the eggs needed for reproduction.
Maternal exposure to polystyrene nanoparticles retarded fetal growth and triggered metabolic disorders of placenta and fetus in mice
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.
Exposure to high dose of polystyrene nanoplastics causes trophoblast cell apoptosis and induces miscarriage
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.
Ferroptosis induced by environmental pollutants and its health implications
Researchers reviewed how environmental pollutants — including microplastics, PM2.5, and heavy metals — trigger ferroptosis, a form of programmed cell death driven by iron and fat oxidation, finding that targeting this cell death pathway could be a strategy to reduce organ damage caused by pollution exposure.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Placental Exposure to Nanoplastics Threatening the Maternal and Fetal Health
This review examines how nanoplastics reaching the placenta threaten maternal and fetal health, summarizing evidence from animal and in vitro studies showing that placental nanoplastic accumulation disrupts nutrient transport, immune function, and fetal development.
Enhanced toxic effects of photoaged microplastics on the trophoblast cells
Researchers investigated how light-aged polystyrene microplastics affect placental function in pregnant mice and found that aged particles caused greater harm than pristine ones. Oral exposure to microplastics starting early in pregnancy impaired fetal growth and damaged the placental tissue layer. The enhanced toxicity of aged microplastics appears to be linked to changes in their physical properties and increased lipid peroxidation in trophoblast cells.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
Ferroptosis Is Involved in Sex-Specific Small Intestinal Toxicity in the Offspring of Adult Mice Exposed to Polystyrene Nanoplastics during Pregnancy
When pregnant mice were exposed to 80-nanometer polystyrene nanoplastics through inhalation, their offspring developed intestinal damage involving oxidative stress and a type of cell death called ferroptosis. Female offspring were more severely affected than males, showing sex-specific vulnerability to prenatal nanoplastic exposure. This study raises concerns that breathing in nanoplastics during pregnancy could harm the developing gut of unborn children, with potentially different effects on boys and girls.
Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage
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.
Biological interactions between nanomaterials and placental development and function following oral exposure
Researchers reviewed animal studies on orally ingested nanomaterials (including nanoplastics) and found that while the placenta is generally an effective barrier preventing fetal transfer, nanomaterials accumulating in placental tissue can impair placental development and function, with potential downstream effects on fetal health.
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
Researchers found that inhaled polystyrene nanoplastics cause lung damage through a specific cell death process called ferroptosis, which involves iron buildup and oxidative stress in lung cells. The nanoplastics damaged mitochondria and triggered a chain reaction where the cell's iron storage was broken down, releasing harmful iron. Blocking this ferroptosis process with a drug called ferrostatin-1 reversed the lung damage in mice, pointing to a potential treatment approach.
Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases
This review explores ferroptosis, a type of iron-dependent cell death that damages brain cells through fat oxidation, and its role in neurodegenerative diseases like Alzheimer's and Parkinson's. While not directly about microplastics, ferroptosis is one of the cellular damage pathways that microplastic exposure can trigger in brain tissue. Understanding how ferroptosis works may help explain how environmental pollutants, including nanoplastics that can cross the blood-brain barrier, contribute to neurological damage.
Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.