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61,005 resultsShowing papers similar to Polycarbonate nanoplastics and the in vitro assessment of their toxicological impact on liver functionality
ClearEnvironmentally relevant UV-light weathering of polystyrene micro- and nanoplastics promotes hepatotoxicity in a human cell line
Researchers found that UV-weathered polystyrene micro- and nanoplastics at environmentally relevant concentrations induced hepatotoxicity in human liver cells and caused significant changes in gene expression related to liver disease pathways.
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.
Exploring the impact of nanoplastics on human hepatic cells: dynamics of internalization and harmful effects in HuH-7 cells
Researchers investigated how nanoplastics are internalized by human liver cancer cells (HuH-7) and assessed the cellular damage that follows, characterizing the dynamics of particle uptake and the resulting cytotoxic effects relevant to hepatic health.
Differences in toxicity induced by the various polymer types of nanoplastics on HepG2 cells
Researchers compared the toxicity of three common nanoplastic types on human liver cells and found that PET (used in bottles) and PVC were significantly more toxic than polystyrene, causing cell death through oxidative stress and a mitochondrial damage pathway. This is important because most toxicity studies have only tested polystyrene, potentially underestimating the health risks of the plastic types people actually encounter most in food and beverage packaging.
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.
In Vitro High-Throughput Toxicological Assessment of Nanoplastics
Researchers developed a high-throughput in vitro method to assess nanoplastic toxicity, finding that laser-ablated polycarbonate and PET nanoparticles showed greater cellular uptake and toxicity than nanoprecipitated PET, highlighting how production method affects nanoplastic hazard.
Ultraviolet-induced photodegradation elevated the toxicity of polystyrene nanoplastics on human lung epithelial A549 cells
Researchers found that UV-induced photodegradation significantly increased the toxicity of polystyrene nanoplastics on human lung epithelial cells. The degraded nanoplastics caused greater cell death, stronger oxidative stress, more severe membrane damage, and intensive mitochondrial dysfunction compared to non-degraded particles, suggesting that weathered nanoplastics in the environment may pose greater health risks than pristine ones.
Nanoplastics and Microplastics May Be Damaging Our Livers
This systematic review summarizes research on how micro- and nanoplastics may damage the liver. Since the liver is the body's main detoxification organ, it plays a key role in processing plastic particles that enter the body through food, water, and air, and the evidence suggests these particles can cause inflammation, oxidative stress, and other liver problems.
Integrated transcriptomic and metabolomic analyses to decipher the regulatory mechanisms of polystyrene nanoplastic-induced metabolic disorders in hepatocytes
Using combined transcriptomic and metabolomic analysis, this study found that polystyrene nanoplastics disrupt lipid and amino acid metabolism in hepatocytes, identifying key regulatory genes and providing data relevant to assessing health risks from nanoplastic exposure.
Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.
Integrated 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.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Nanoplastics Toxicity Specific to Liver in Inducing Metabolic Dysfunction—A Comprehensive Review
This review examines how nanoplastics, particles smaller than 100 nanometers, accumulate in and damage the liver. Researchers found that nanoplastics enter the body through the respiratory and digestive systems, reach the liver via the bloodstream, and can disrupt the gut-liver axis and gut microbiome. The evidence suggests that liver damage from nanoplastics may trigger cascading effects on other organs, highlighting the need for further research on these less visible pollutants.
The effects of concentration, duration of exposure, size and surface function of polymethyl methacrylate micro/nanoplastics on human liver cells
Researchers tested the effects of polymethyl methacrylate micro- and nanoplastics on human liver cells, varying the particle concentration, exposure duration, size, and surface chemistry. They found that smaller particles and those with specific surface modifications caused greater cellular damage, including reduced viability and increased oxidative stress. The study suggests that the physical and chemical properties of microplastics play a critical role in determining their potential toxicity to human tissues.
Hepatotoxic mechanisms of functionalized nanopolystyrene: decoding the role of ionic surface groups
Researchers exposed mice to polystyrene nanoplastics with different surface charges via drinking water, finding that charged particles accumulate in liver sinusoids and induce hepatocyte ferroptosis through an endoplasmic reticulum stress cascade, while neutral particles cause endothelial cell senescence through lysosomal dysfunction.
Effects of polystyrene micro/nanoplastics on liver cells based on particle size, surface functionalization, concentration and exposure period
Researchers systematically studied the effects of polystyrene micro- and nanoplastics on human liver cells, varying particle size, surface chemistry, concentration, and exposure duration. They found that smaller particles were internalized more readily and that surface functionalization significantly influenced toxicity, with aminated particles causing the most cell damage. The study suggests that particle characteristics beyond just size play an important role in determining how micro- and nanoplastics affect human cells.
The combined toxicity of polystyrene nano/micro-plastics and triphenyl phosphate (TPHP) on HepG2 cells
This study found that polystyrene nanoplastics and microplastics made a common flame retardant chemical (TPHP) more toxic to human liver cells than the chemical alone. The nanoplastics absorbed the flame retardant and delivered it to cells, causing increased oxidative stress, mitochondrial damage, and cell death. Smaller nanoplastics caused more harm than larger microplastics, suggesting that as plastics break down into smaller pieces, their ability to carry toxic chemicals into human cells increases.
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.
Fate of polystyrene and polyethylene nanoplastics exposed to UV in water
Researchers found that UV irradiation progressively degrades polystyrene and polyethylene nanoplastics dispersed in water, causing them to become porous, fragment, and ultimately degrade completely, revealing the photochemical fate of nanoplastics in sunlit aquatic environments.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Adverse Effect of Polystyrene Nanoplastics in Impairing Glucose Metabolism in Liver Injury
Polystyrene nanoplastics disrupted glucose metabolism in liver cells by interfering with insulin signaling pathways and mitochondrial function, suggesting that nanoplastic exposure could contribute to metabolic disorders including insulin resistance.
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.
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.
Long-Term Exposure to Polystyrene Nanoplastics Impairs the Liver Health of Medaka
Researchers found that three months of exposure to polystyrene nanoplastics caused significant liver damage in medaka fish, including oxidative stress, immune disruption, and altered gene expression related to lipid metabolism and detoxification pathways.