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The Mechanism of Combined Exposure of Polystyrene Microplastics and Cadmium Inducing Hepatic Injury through the Modulation of PI3K/AKT/mTOR-Mediated Autophagy
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Researchers examined liver damage in mice exposed to polystyrene microplastics and cadmium, both alone and in combination, and found that triple exposure to 100-nanometer particles, 1-micrometer particles, and cadmium caused the most severe liver dysfunction. The study suggests that nanoscale microplastics significantly enhance cadmium-induced liver injury through disrupted autophagy via the PI3K/AKT/mTOR signaling pathway.
Recent studies indicate that microplastics and nanoplastics (MNPs) act as key vectors for contaminants including cadmium (Cd). However, the bioavailability induced by their interaction remains controversial. Since both MNPs and Cd primarily accumulate in the liver after ingestion by organisms, hepatotoxicity induced by coexposure to MNPs (100 mg/kg body weight (BW)), 100 nm and 1 μm polystyrene (PS), and Cd (5 mg/kg BW) was examined in this study. Single or combined exposure models were established, and gavage was performed 5 times a week for 5 weeks. We observed that polystyrene (PS) accumulated in the mice liver. In comparison to the control group, all exposure groups exhibited significantly increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, altered hepatic antioxidant enzyme activities, decreased P62 protein expression, and elevated Beclin-1 expression and LC3II/I ratios, indicating that PS alone or in combination with Cd disrupted liver structures and induced excessive autophagy and oxidative damage. Specifically, the 1 μm PS group induced significantly stronger hepatotoxic effects than the 100 nm PS group. In contrast, for 100 nm PS, although it was less toxic when administered alone, it significantly enhanced the Cd-induced liver injury. Notably, triple exposure to 100 nm PS, 1 μm PS, and Cd resulted in the most severe liver dysfunction, histopathological alterations, and activated cellular autophagy. Mechanistic investigations revealed that PS exposure alone or in combination with Cd triggered excessive autophagy and oxidative stress in hepatocytes by interfering with the PI3K/AKT/mTOR signaling pathway, thereby mediating liver injury. This study innovatively demonstrates that coexposure to different-sized PS particles and Cd can lead to complex liver injury patterns while particle size influences their combined hepatotoxicity with Cd.
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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.
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Scientists found that when tiny plastic particles and the toxic metal cadmium are combined, they cause more damage to liver cells than either pollutant alone. The plastic particles help cadmium get into cells more easily, leading to harmful changes in the cell's powerhouses (mitochondria) and increased cell death. While this study used duck cells, it suggests that the growing presence of microplastics in our environment could make heavy metal pollution more dangerous to human health.
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Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Transcriptomic and Metabolomic Analysis Reveals That Polystyrene Microplastics Exacerbate Cadmium-Induced Liver Damage in Mice Associated with AMPK-FOXO-Mediated Energy Metabolism Dysregulation
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A new mouse study found that microplastics can make cadmium (a toxic heavy metal found in some foods and pollution) even more damaging to the liver than cadmium alone—causing worse liver injury, more inflammation, and disrupted energy production inside liver cells. This matters because we're regularly exposed to both microplastics and heavy metals in our environment and food, and this research suggests these pollutants may combine to harm our health in ways that studying them separately wouldn't reveal. While this was done in mice and not humans, it raises important questions about the real-world risks of everyday exposure to multiple pollutants at once.
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This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
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