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Mitigation of polystyrene microplastic-induced hepatotoxicity in human hepatobiliary organoids through bile extraction
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Using lab-grown human liver organoids, researchers discovered that polystyrene microplastics accumulate in bile ducts and cause liver cell damage. They found that a bile acid medication called ursodeoxycholic acid actually helped move microplastics into bile ducts for removal, while blocking bile transport made the liver damage worse. This study suggests that the body's bile system may play a role in clearing microplastics from the liver, pointing toward potential treatment strategies.
BACKGROUND & AIMS: Polystyrene microplastics (PS-MPs) are pervasive in our daily life and can be ingested by the human body through bioaccumulation, causing organ damage, especially liver damage. However, the effect of PS-MPs bioaccumulation on human hepatotoxicity and their metabolism remains unclear. Recent studies have demonstrated that PS-MPs cause lipid and bile acid metabolism disorders. The human hepatobiliary organoids (HBOs) regenerated from chemically induced liver progenitor cells converted by mature hepatocytes and the bile duct provides a bioengineering model for liver disease and hepatic metabolism. APPROACH & RESULTS: Exposure of HBOs to PS-MPs with a diameter of 1 µm for 48 h causes hepatotoxicity, hepatocyte damage, and changes in bile acid metabolism. PS-MPs could be accumulated into the bile ducts of HBOs, which can be promoted by ursodeoxycholic acid, increasing bile flow and volume by activating the bile transporter of BSEP in a dose-dependent manner along with MRP-2. The accumulation of PS-MPs in the bile duct was able to be inhibited by the bile transporter inhibitor of troglitazone that could inhibit the transporters of BSEP and MRP-2, which increased the hepatotoxicity caused by PS-MPs. CONCLUSIONS: This study provides insights into the metabolic pathways of PS-MPs in the liver and suggests potential therapeutic strategies to reduce MP-induced liver damage.
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Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
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Using an advanced gut-liver organ-on-a-chip system that mimics human digestion, researchers tracked how polystyrene microplastics travel from the intestine to the liver. The microplastics crossed the intestinal barrier, accumulated in liver tissue, and caused dose-dependent damage to liver cells. This human-relevant model provides strong evidence that microplastics ingested through food and water can reach and harm the liver.
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Environmental microplastics and liver health: Brief review on human exposure and accumulation, hepatotoxicity mechanism, and intervention strategies
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