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61,005 resultsShowing papers similar to Polystyrene microplastics up-regulates liver glutamine and glutamate synthesis and promotes autophagy-dependent ferroptosis and apoptosis in the cerebellum through the liver-brain axis
ClearActivation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
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.
Dose-dependent alteration in hepatic and cerebral glucose metabolism following exposure to polystyrene microplastic in Wistar rats
Researchers exposed Wistar rats to polystyrene microplastics and observed dose-dependent changes in glucose metabolism in both the liver and brain. The study suggests that microplastic exposure may disrupt normal metabolic processes, with higher doses leading to more pronounced alterations in hepatic and cerebral glucose handling.
The effects of microplastics exposure on quail's hypothalamus: Neurotransmission disturbance, cytokine imbalance and ROS/TGF-β/Akt/FoxO3a signaling disruption
Japanese quail exposed to polystyrene microplastics for five weeks showed significant brain damage in the hypothalamus, including structural changes to neurons, disrupted chemical signaling, and inflammation. The microplastics caused oxidative stress and interfered with important cell-survival pathways in the brain. While studied in birds, these neurotoxic effects are relevant because similar brain pathways exist in humans, and they suggest microplastic exposure could affect neurological function.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
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.
Impact of the Oral Administration of Polystyrene Microplastics on Hepatic Lipid, Glucose, and Amino Acid Metabolism in C57BL/6Korl and C57BL/6-Lepem1hwl/Korl Mice
Researchers investigated the effects of orally administered polystyrene microplastics on liver metabolism in normal and obese mice over eight weeks. They found that microplastic exposure altered lipid, glucose, and amino acid metabolism pathways in the liver and adipose tissues. The study suggests that microplastic ingestion may disrupt hepatic metabolic functions, with potentially different impacts depending on baseline metabolic health status.
Microplastic-mediated new mechanism of liver damage: From the perspective of the gut-liver axis
This review describes how microplastics can damage the liver through the gut-liver axis: they first disrupt the gut's protective barrier and beneficial bacteria, allowing harmful substances to leak through the weakened intestinal wall into the bloodstream and travel to the liver. Once there, these substances cause inflammation, metabolic problems, and oxidative stress, offering a new explanation for how microplastic exposure could lead to liver disease.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
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.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
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.
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.
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.
Revealing transport, uptake and damage of polystyrene microplastics using a gut-liver-on-a-chip
Using an advanced gut-liver organ-on-a-chip system that mimics human digestion, researchers tracked how polystyrene microplastics travel from the intestine to the liver. The microplastics crossed the intestinal barrier, accumulated in liver tissue, and caused dose-dependent damage to liver cells. This human-relevant model provides strong evidence that microplastics ingested through food and water can reach and harm the liver.
Association between long-term exposure of polystyrene microplastics and exacerbation of seizure symptoms: Evidence from multiple approaches
This study found that long-term exposure to polystyrene microplastics may worsen seizure symptoms by disrupting gut bacteria and triggering inflammation that damages brain cells. Using both human data and animal experiments, the researchers showed that microplastics can set off a chain reaction from the gut to the brain, leading to a type of cell death called ferroptosis in the hippocampus. The findings suggest that chronic microplastic exposure could be a hidden risk factor for people with seizure disorders.
Microplastics in focus: a silent disruptor of liver health- a systematic review
This systematic review examines how micro- and nanoplastics affect liver health, based on 25 experimental and observational studies. The evidence shows that polystyrene particles can cause liver inflammation, oxidative stress, fat buildup, and disruption of metabolic pathways. These findings are concerning because the liver is the body's primary detoxification organ, and plastic-related damage could impair its ability to process other toxins.
Transcriptomic and metabolomic analysis reveals hepatic lipid metabolism disruption in Japanese quail under polystyrene microplastics exposure
Researchers fed Japanese quail polystyrene microplastics at environmentally relevant concentrations for 35 days and analyzed liver effects using transcriptomics and metabolomics. Low doses caused increased food intake and weight gain with liver lipid accumulation, while high doses led to decreased intake and weight loss, suggesting a hormetic dose-response pattern. The study found that microplastic exposure disrupted hepatic lipid metabolism pathways and caused liver oxidative stress in birds.
New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.
Dose-effect of polystyrene microplastics on digestive toxicity in chickens (Gallus gallus): Multi-omics reveals critical role of gut-liver axis
Researchers fed chickens different doses of polystyrene microplastics and used multi-omics analysis to study digestive system damage through the gut-liver axis. They found that microplastics disrupted gut barrier function, altered liver metabolism, and changed gut bacterial communities in a dose-dependent manner. The study provides detailed molecular evidence of how microplastics can damage the digestive health of poultry, which may have implications for food safety.
Gut microbiota dysbiosis exacerbates polystyrene microplastics-induced liver inflammation via activating LPS/TLR4 signaling pathway in ducks
This study found that polystyrene microplastics exacerbate gut microbiota dysbiosis in ducks, and that this disruption of the gut microbial community amplifies liver inflammation through the gut-liver axis, revealing a mechanism by which MP exposure causes hepatic injury.
Polystyrene microplastics trigger hepatocyte apoptosis and abnormal glycolytic flux via ROS-driven calcium overload
This study investigated how polystyrene microplastics damage liver cells and found they trigger a chain reaction involving excess reactive oxygen species (ROS) that leads to calcium overload inside cells. The calcium buildup disrupts normal energy metabolism and ultimately causes liver cell death. The findings reveal a specific molecular pathway connecting microplastic-driven oxidative stress to liver toxicity.
Polystyrene Microplastics and Cadmium Drive the Gut-Liver Axis Through the TLR4/MyD88/NF-κB Signaling Pathway to Cause Toxic Effects on Broilers
Broiler chickens exposed to polystyrene microplastics and cadmium, both commonly found in contaminated feed, developed intestinal damage and liver inflammation. The pollutants disrupted gut barrier proteins, altered intestinal bacteria, and triggered an inflammatory immune pathway in the liver. This is relevant to human health because it demonstrates how microplastics and heavy metals in the food chain can damage the gut-liver connection in poultry, potentially affecting the safety of chicken as food.