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61,005 resultsShowing papers similar to Chronic Microplastic Exposure Dose‐Dependently Induces Liver Failure via Oxidative Stress, Inflammation, and Apoptosis in Rats
ClearExploring the Impacts of Polyethylene Microplastics on Rat Liver
Wistar rats exposed to polyethylene microplastics at 0.1–5 mg/kg for 4 weeks showed dose-dependent PE accumulation in liver tissue confirmed by fluorescence microscopy, with histopathological signs of liver injury despite no significant change in body weight.
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.
In vivo test of acute exposure of polyethylene microplastics on kidney and liver of Rattus norvegicus Wistar strain rats
Researchers exposed male rats to a single dose of polyethylene microplastics and monitored them for 14 days, finding significant changes in body weight, elevated markers of kidney and liver stress in blood tests, and visible tissue abnormalities under microscopy. The results indicate that even short-term, high-dose microplastic exposure can cause measurable organ damage in mammals.
Dose‐Dependent Toxicological Effects of Polyvinyl Chloride and Polystyrene Microplastics on Wistar Albino Rats
Researchers fed rats PVC and polystyrene microplastics at different doses for eight weeks and observed significant changes including weight loss, elevated blood glucose, increased cholesterol and liver enzymes, and signs of oxidative stress. The study suggests that oral microplastic exposure at these levels can cause dose-dependent toxicological effects across multiple organ systems in mammals.
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.
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.
Acute Toxicity Assessment of Orally Administered Microplastic Particles in Adult Male Wistar Rats
Researchers gave adult male rats a single oral dose of microplastics made from PET water bottles and found that even this one-time exposure altered markers of liver, heart, and kidney function. Higher doses also reduced food intake and increased signs of oxidative stress, which is cell damage caused by harmful molecules. This study suggests that even brief microplastic exposure could trigger early changes in organ function, raising questions about the cumulative effect of daily human exposure through food and water.
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.
Nanoplastics, Liver Injury, and Oxidative Mechanisms: Translating Animal Models Into Human Risk Assessment
This scoping review synthesized evidence from animal studies on how micro- and nanoplastics cause liver injury, focusing on the underlying mechanisms of toxicity. Researchers found that oxidative stress is a principal pathway by which these particles damage liver tissue, and the study evaluates what these preclinical findings may mean for assessing human health risks from plastic particle exposure.
Microplastic-induced hepatic adverse effects evaluated in advanced quadruple cell human primary models following three weeks of repeated exposure
Scientists tested the effects of microplastics on a sophisticated model of human liver cells over three weeks of repeated exposure, finding that certain microplastic types triggered inflammation and altered liver function. The advanced cell model, which combines four types of human liver cells, provides more realistic results than simpler lab tests. These findings add to growing evidence that microplastics accumulating in the liver could contribute to chronic inflammation and liver damage in humans.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study
Researchers fed immature piglets PET microplastics for four weeks and examined the effects on their livers. They found that microplastic exposure altered gene expression patterns related to metabolism and immune response, and increased markers of oxidative stress in the liver. The study suggests that even relatively short-term microplastic ingestion may disrupt liver function at the molecular level.
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.
Renal and Hepatotoxic Effects of Polyethylene Terephthalate Microplastics in Chronically Exposed Albino Rats
Researchers exposed albino rats to different doses of PET microplastics for 90 days and measured kidney and liver function markers. They found that chronic exposure led to significant changes in serum urea, creatinine, and liver enzymes, suggesting potential kidney and liver damage at higher doses. The study also found that water stored in PET containers exposed to sunlight showed similar toxic effects, raising concerns about everyday plastic container use.
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.
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.
Chronic PET‐Microplastic Exposure: Disruption of Gut–Liver Homeostasis and Risk of Hepatic Steatosis
Researchers exposed mice to PET microplastics ground from plastic bottles over 29 weeks and found that the particles caused obesity, liver enlargement, fatty liver disease, and early-stage scarring of liver tissue. The microplastics also disrupted gut bacteria and bile acid metabolism, pointing to damage along the gut-liver connection. The findings raise concerns about the long-term health effects of chronic exposure to the type of microplastics commonly found in food and beverages.
Impact of microplastics exposure on liver health: A comprehensive meta-analysis
This meta-analysis of 70 studies across mice, fish, crabs, and shrimp found that microplastic exposure significantly increases liver enzymes (ALT, AST), oxidative stress marker MDA, and pro-inflammatory cytokines (IL-6, TNF-alpha), while reducing protective antioxidant enzymes (SOD, CAT, GSH, GPx). The findings demonstrate that microplastics disrupt liver function through oxidative stress and inflammation across multiple animal species.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.
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.
Liver Injury Induced by Exposure to Polystyrene Microplastics Alone or in Combination with Cadmium in Mice Is Mediated by Oxidative Stress and Apoptosis
Researchers exposed mice to polystyrene microplastics alone and combined with cadmium over eight weeks to study liver damage. Both exposures caused liver injury through oxidative stress and programmed cell death, but the combination of microplastics and cadmium produced more severe effects. The study suggests that microplastics may worsen the toxic impact of heavy metals on the liver when both are present together.
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.
Evaluation of Liver Function Through SGOT and SGPT Quantification in Rats Administered Polyethylene Terephthalate Microplastics
Researchers administered PET microplastics orally to white rats at doses of 0.4–1.0 mg/day and measured SGOT and SGPT liver enzyme levels, finding dose-dependent increases in both transaminases indicating hepatotoxicity even at low exposure levels.