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Evaluating the Hepatotoxicity of Polyvinyl Chloride Microplastics in Ducks: Oxidative andFibrotic Outcomes
Summary
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.
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease that is common world-wide and studied extensively in mammals.Nevertheless, the pathways of NAFLD associated liver damage in the digestive tracts of birds remain unclear.In this study, 7-day-old female Muscovy ducks of the same batch were split into three groups and were fed pure water, 1mg/L polyvinyl chloride microplastics (PVC-MPs) or 10mg/L PVC-MPs, respectively, for 2 months.This study aimed to verify whether oxidative stress originated from PVC-MPs resulted in NAFLD in duck liver, thus triggering apoptosis in hepatocytes.The results of the study proved that the accumulation of PVC-MPs in liver had adverse effects on the morphological structure and functional performance of liver cells.This finding was supported by a decrease of liver organ coefficient and pathological injury to liver cells, as well as ultrastructural injury.Oxidative stress injury in the liver of female breeding duck induced the deficiency of PCK1 and activated PI3K/AKT pathway, which resulted in fatty deposition and fibrosis in the liver and led to hepatocyte apoptosis.In conclusion, PVC-MPs induced hepatic oxidative damage, hepatic lipid deposition and hepatic tissue fibrosis, and hence hepatic apoptosis.Our research provides new perspectives on the association of PVC-MPs with liver toxicity in female duck that contains hepatic dysfunction, mainly NAFLD.