We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
ClearIntegrated transcriptomics and metabolomics to explore the varied hepatic toxicity induced by aged- and pristine-microplastics: in vivo and human-originated liver organoids-based in vitro study
Using human liver organoids (miniature lab-grown livers), researchers found that sun-aged microplastics caused more damage to liver cells than fresh microplastics, even at concentrations matching what is found inside human bodies. The aged particles specifically disrupted energy production in mitochondria and altered an amino acid metabolism pathway linked to cardiovascular disease. This is significant because most microplastics in the environment have been weathered by sunlight, meaning the real health risk may be greater than studies using pristine plastics suggest.
Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.
The iron matters: Aged microplastics disrupted the iron homeostasis in the liver organoids
Researchers compared the effects of fresh versus aged polystyrene microplastics on lab-grown human liver tissue and found that aged particles caused significantly more damage. The aged microplastics disrupted iron balance in liver cells, leading to a form of cell death called ferroptosis, and triggered inflammatory responses. The study suggests that weathered microplastics encountered in everyday life may pose greater risks to liver health than the pristine particles typically used in laboratory studies.
Photoaged polystyrene nanoplastics induce perturbation of glucose metabolism in HepG2 cells via oxidative stress
Researchers exposed human liver cells to polystyrene nanoplastics with varying degrees of UV-induced aging and found that photoaged particles caused more severe disruptions to glucose metabolism than pristine ones. Long-term photoaged nanoplastics triggered dose-dependent metabolic disorders through oxidative stress, while pristine particles only caused effects at high concentrations. The study suggests that weathered nanoplastics in the environment may pose greater health risks than fresh plastic particles.
Microcystins-Loaded Aged Nanoplastics Provoke a Metabolic Shift in Human Liver Cells
Researchers found that aged polystyrene nanoplastics can adsorb significantly more microcystin toxins than pristine nanoplastics, and the toxin-loaded particles caused greater harm to human liver cells. The combined exposure triggered metabolic energy disruption, oxidative damage, and stress in cellular machinery. The study suggests that environmentally weathered nanoplastics may pose amplified health risks by carrying higher loads of harmful waterborne toxins.
Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.
New Insights into the Mechanisms of Toxicity of Aging Microplastics
This study showed that UV-aged polypropylene microplastics are significantly more toxic than fresh ones, absorbing more chemicals and generating more harmful reactive oxygen species in seawater. The aged particles caused greater damage to cell membranes in mussels compared to pristine plastics. Since most microplastics in the ocean have been weathered by sunlight, real-world exposure risks may be higher than laboratory studies using new plastics suggest.
Unraveling the impacts of photolysis-induced aging microplastics on enhanced immunotoxicity and nephrotoxicity
Researchers compared the toxicity of pristine and sun-aged polyethylene and PET microplastics on kidney cells and immune cells and found that aged particles were up to 40 percent more toxic. The increased harm was attributed to environmentally persistent free radicals that form on plastic surfaces during UV exposure, which amplify oxidative stress inside cells. The study highlights that weathered microplastics in the real environment may pose greater health risks than the pristine particles typically used in laboratory studies.
Potential toxicity of microplastics on vertebrate liver: A systematic review and meta–analysis
This meta-analysis of 118 studies found that microplastics damage vertebrate livers by inducing oxidative stress and intracellular toxicity, altering biotransformation processes, and disrupting lipid metabolism. Organisms at earlier life stages, exposed to smaller particles, and for longer durations showed the greatest liver damage, with catalase, GST, reactive oxygen species, and alkaline phosphatase levels progressively increasing with microplastic concentration.
Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver.
Mice fed polyethylene microplastics in their food for 6 to 9 weeks developed liver inflammation, metabolic disruption, oxidative stress, and increased cell growth in the liver. The microplastics also worsened liver scarring (fibrosis) when tested in mice with pre-existing liver damage. This is the first study to show that ingesting polyethylene, the most common type of plastic, can directly damage the mammalian liver and could worsen existing liver conditions.
Enhanced hepatic metabolic perturbation of polystyrene nanoplastics by UV irradiation-induced hydroxyl radical generation
Researchers found that ultraviolet light exposure changes the surface properties of polystyrene nanoplastics, making them more toxic to mouse livers than untreated particles. The UV-altered nanoplastics caused greater disruption to liver metabolism, triggering increased oxidative stress and inflammatory responses. The study highlights that environmental weathering can make nanoplastics more harmful over time, which means laboratory studies using pristine particles may underestimate real-world health risks.
Impact of environmental microplastic exposure on HepG2 cells: unraveling proliferation, mitochondrial dynamics and autophagy activation
Lab experiments on human liver cells found that exposure to common microplastics (polyethylene and PET) increased cell growth but also triggered oxidative stress, damaged mitochondria (the cell's energy centers), and activated autophagy -- a process where cells try to clean up internal damage. These findings suggest that microplastics may disrupt normal liver cell function in ways that could have long-term health consequences.
Impact of aged and virgin polyethylene microplastics on multi end-points effects of freshwater fish tissues
Freshwater fish exposed to polyethylene microplastics for 15 days showed increased oxidative stress in both liver and muscle tissue, with aged, UV-weathered microplastics causing more damage than new ones. The weathering process changed the plastic surface in ways that made the particles more chemically reactive and potentially more harmful. This matters because microplastics in the environment are typically aged, meaning lab studies using only pristine particles may underestimate real-world toxicity.
Kidney and Liver Disorders Due to Microplastic Exposure: Chronic in Vivo Study in Male White Rats
Male white rats were chronically exposed to microplastics (particles 5 mm or smaller) to assess kidney and liver toxicity, with exposure resulting from environmental weathering and ultraviolet irradiation of plastic materials. The study found measurable histopathological and biochemical damage in both organs, confirming that long-term microplastic exposure causes organ-level injury in mammals.
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.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
UVB-aged microplastics and cellular damage : An in vitro study
Researchers conducted in vitro experiments to assess whether UVB-aged microplastics cause greater cellular damage than unaged plastics, given that UV irradiation fragments and chemically alters plastic surfaces. The study found that UVB aging enhanced the capacity of microplastics to cause cellular toxicity.
Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size
Researchers exposed mouse liver cells to polystyrene microplastics of different sizes and found that smaller particles caused more oxidative stress and damage than larger ones. The microplastics disrupted protective antioxidant systems and increased harmful reactive oxygen species inside the cells. This suggests that the smallest microplastic particles may pose the greatest risk to liver health because they can enter cells more easily and cause more internal damage.
Emerging threat of environmental microplastics: A comprehensive analysis of hepatic metabolic dysregulation and hepatocellular damage (Review)
This review summarizes existing research on how microplastics damage the liver, which is a key organ for filtering toxins from the body. Studies show that microplastics can cause liver tissue damage, trigger cell death, and disrupt fat metabolism, with smaller particles and longer exposure causing worse effects. The findings highlight the liver as a particularly vulnerable organ because it accumulates microplastics that enter the body through food and water.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
Chronic Microplastic Exposure Dose‐Dependently Induces Liver Failure via Oxidative Stress, Inflammation, and Apoptosis in Rats
This animal study found that chronic exposure to polyethylene microplastics caused dose-dependent liver damage in rats over just four weeks. Higher doses led to increased markers of liver injury, oxidative stress, inflammation, and cell death, suggesting that ongoing microplastic ingestion could harm liver health over time.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.