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Polystyrene Nanoplastics and Cadmium Co-Exposure Accelerates Mitochondrial Autophagy Mediated by HSP60–SIRT3–SOD 2 Signaling Pathway in Primary Duck Embryo Hepatocytes
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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.
Microplastics (MPs) in the environment frequently act as a medium to adsorb heavy metals and antibiotics. This combined exposure often has a greater effect on animal toxicity than exposure alone. However, there is a paucity of research focusing on the combined toxicity of nanoplastics (NPs) and heavy metals when coexposed to hepatocytes in poultry. In this study, the effects of PS-NPs (0.08 μm, 10 μg/mL) and cadmium chloride (CdCl2) (4 μg/mL) on duck hepatocytes and their mechanisms were observed using primary duck embryo hepatocytes (PDEH) cells as an in vitro model. The results demonstrated that Cd exposure exacerbated the accumulation of PS-NPs in PDEH cells, likely due to the formation of pores on the cell membrane surface. The addition of the antioxidant N-Acetyl-l-cysteine (NAC) significantly reduced the uptake of PS-NPs by PDEH cells. PDEH cells in the coexposed group exhibited significantly abnormal morphology and diminished cell number and survival rate. Furthermore, exposure to PS-NPs exacerbated Cd-mediated oxidative stress and mitochondrial autophagy damage in duck hepatocytes. The restoration of these injuries was observed in response to intervention with the SIRT3 activator (NRCL, 2 ng/mL). Immunoprecipitation experiments demonstrated that the SIRT3 protein interacted with the SOD2 protein. The present study found that co-exposure of PS-NPs+Cd induced mitochondrial autophagy in PDEH cells, which may be mediated by the HSP60/SIRT3/SOD2 signaling axis. It is hoped that these findings will provide new ideas for combating the mechanism of microplastics and Cd-induced hepatotoxicity in poultry.
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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.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
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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.
Liver Injury Induced by Exposure to Polystyrene Microplastics Alone or in Combination with Cadmium in Mice Is Mediated by Oxidative Stress and Apoptosis
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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.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
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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.
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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