We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38 MAPK/p65 NF‐κB Signaling Pathway
Summary
Researchers found that exposure to PET microplastics induced liver fibrosis in mice through oxidative stress and activation of the p38 MAPK/p65 NF-kB signaling pathway. The study suggests that PET microplastics, which are frequently detected in both environmental samples and human tissues, may contribute to liver damage through inflammatory and oxidative mechanisms.
Microplastic (MP) pollution has garnered attention due to its potential impact on living organisms. Among these, polyethylene terephthalate microplastics (PET-MPs) are frequently detected in both environmental samples and human tissues. Despite this, the effects of PET-MPs on liver damage and fibrosis in mammals remain insufficiently understood. This study demonstrated that oral exposure to PET-MPs at doses of 1 mg/day (with a diameter of 1 μm) over 42 days resulted in inhibited weight gain and altered organ coefficients in male mice, suggesting possible liver damage. Using HE and Masson staining revealed pathological changes in the livers of exposed mice, such as hepatocyte swelling, inflammatory cell infiltration, and collagen deposition. Liver function tests confirmed elevated serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Further, the elevated levels of oxidative stress markers, along with the enhanced expression of proteins related to the p38 MAPK/p65 NF-κB signaling pathway as revealed by western blot analysis, both of which are strongly associated with liver damage and fibrosis. To further elucidate these mechanisms, experiments involving N-acetylcysteine (NAC) to counteract oxidative stress and SB203580 to inhibit p38 MAPK activation demonstrated that both interventions effectively mitigated liver fibrosis. Exposure to PET-MPs may trigger liver injury and fibrosis in mice. During this process, oxidative stress and the p38 MAPK/p65 NF-κB signaling pathway may play significant mediating roles.
Sign in to start a discussion.
More Papers Like This
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.
Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice
Researchers fed mice polystyrene nanoplastics and found that the particles disrupted the animals' ability to regulate blood sugar and fat metabolism. The nanoplastics triggered oxidative stress and inflammation in the liver, activating signaling pathways that led to insulin resistance and abnormal fat accumulation. The study provides evidence that nanoplastic exposure may contribute to metabolic disorders through specific molecular mechanisms involving the NF-kB and MAPK pathways.
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.
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.
In vivo hepatic effects and post-exposure recovery following polyethylene terephthalate microplastic ingestion in Swiss Albino mice (Mus musculus)
Researchers exposed Swiss Albino mice to two concentrations of PET microplastics for 14 days via drinking water, finding significant liver enzyme disruption and oxidative stress markers, followed by a 7-day depuration period that showed partial recovery of some but not all biomarkers.