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Co-exposure of polyvinyl chloride microplastics with cadmium promotes nonalcoholic fatty liver disease in female ducks through oxidative stress and glycolipid accumulation
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Researchers found that female ducks exposed to both PVC microplastics and cadmium together developed nonalcoholic fatty liver disease, with the combination being worse than either pollutant alone. The co-exposure caused oxidative stress and abnormal fat and sugar buildup in the liver. This study is relevant to human health because people are also exposed to microplastics and heavy metals simultaneously, and the combined effects may be more damaging than exposure to either one individually.
A recently discovered environmental contaminant, microplastics (MP) are capable of amassing within the body and pose a grave threat to the health of both humans and animals. It is widely acknowledged that the combination of cadmium (Cd), a hazardous heavy metal, and microplastics produces synergistic deleterious effects. Nevertheless, the mechanism by which co-exposure to polyvinyl chloride microplastics (PVC-MP) and Cd damages the liver of avian females is unknown. Globally prevalent and the subject of extensive research in mammals, nonalcoholic fatty liver disease (NAFLD) is a chronic liver condition. However, the mechanisms underlying injury to the avian digestive system caused by NAFLD remain unknown. Two months of co-exposure to Cd and PVC-MPs, pure water, solitary Cd exposure, single microplastics exposure, and pure water were administered to female Muscovy ducks in this study. The objective of this research was to examine whether the co-exposure of duck liver to PVC-MPs and Cd-induced oxidative stress resulted in NAFLD and subsequent apoptosis of hepatic cells. The study's findings showed that hepatocyte shape and functional activity were negatively impacted by PVC-MP and Cd buildup in liver tissues. Reduced liver organ coefficients, increased alanine aminotransferase (ALT) content, and ultrastructural damage to hepatocyte nuclei and mitochondria are indicators of this. These results point to a possible impairment in liver function. phosphoenolpyruvate carboxykinase 1 (PCK1) deficiency activates the protein kinase B/phosphatidylinositol 3-kinase (PI3K/AKT) pathway in the livers of female reproductive ducks that have been damaged by oxidative stress. This stimulation induces lipid deposition, fibrosis, and glycogen accumulation, which ultimately results in hepatocyte apoptosis. In summary, our research provides evidence that PVC-MPs cause oxidative harm to the liver, which subsequently results in fibrosis of liver tissue, hepatic glucolipid metabolism, and ultimately apoptosis.
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Co-exposure to PVC microplastics and cadmium induces oxidative stress and fibrosis in duck pancreas
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Researchers found that exposing ducks to PVC microplastics and cadmium together caused far worse pancreatic damage than either pollutant alone, including severe inflammation, fibrosis, and disrupted organ function. The combined exposure overwhelmed the ducks' antioxidant defenses and caused mitochondrial damage in pancreatic cells. Since waterfowl are highly exposed to both microplastics and heavy metals in contaminated waterways, this study shows how these common pollutants can interact to amplify organ damage.
Molecular regulatory networks of microplastics and cadmium mediated hepatotoxicity from NAFLD to tumorigenesis via integrated approaches
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This study mapped out how microplastics and the toxic metal cadmium work together to damage the liver, tracing a progression from fatty liver disease to cirrhosis and eventually liver cancer. Cadmium activates genes linked to cell growth and tumor formation, while microplastics trigger cell death pathways related to inflammation. When combined, the two pollutants accelerate liver damage more than either one alone, raising concerns about real-world exposure where people encounter both simultaneously.
Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice
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Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
Evaluating the Hepatotoxicity of Polyvinyl Chloride Microplastics in Ducks: Oxidative andFibrotic Outcomes
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Researchers fed ducks low and high doses of polyvinyl chloride (PVC) microplastics for two months and found that the particles accumulated in the liver, causing fat buildup, scarring, and cell death — similar to fatty liver disease in humans — suggesting plastic pollution may harm bird liver health in ways previously only studied in mammals.
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.
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