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Co-exposure to F-53B and nanoplastics induced hepatic glucolipid metabolism disorders by the PI3K-AKT signaling pathway
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Researchers studied the combined effects of the industrial chemical F-53B and nanoplastics on liver function in mice over two months. They found that co-exposure caused liver swelling and disrupted both fat and sugar metabolism through a specific signaling pathway, with effects more severe than either substance alone. The study suggests that nanoplastics may enhance the liver toxicity of fluorinated industrial chemicals by increasing their accumulation in the body.
Recent investigations suggest that the chemical compound F-53B (6:2 chlorinated polyfluorinated ether sulfonate) may pose risks of liver toxicity. Within environmental settings, F-53B attaches to microplastics and nanoplastics, which are capable of being consumed by diverse species. To investigate the synergistic effects on hepatotoxicity, adult male mice were subjected to F-53B at daily doses of 1, 10, and 100 μg/kg, NPs at 100 mg/kg per day, or a combination of both treatments for a duration of 2 months. The results indicated that NPs moderately increased the buildup of F-53B within both the liver and plasma. Co-exposure to F-53B (100 μg/kg/day) and NPs induced hepatocellular edema and elevated plasma ALT levels, which were rarely observed in groups exposed to F-53B or NPs alone. Additionally, we found that co-exposure decreased the concentrations of total cholesterol (TC) and triglycerides (TG) in both plasma and liver tissues, while increasing fasting plasma glucose and insulin levels. Transcriptomic analysis revealed that the PI3K-AKT signaling pathway is potentially involved in mediating hepatic metabolic disorders. Further experiments demonstrated that the combined treatment significantly suppressed the expression of FGF21, an upstream regulator of the PI3K-AKT pathway. This alteration resulted in the suppression of PI3K-regulated gene expression associated with glucose and lipid metabolism. The findings suggest that F-53B impairs hepatic glucolipid metabolism in mice by suppressing of the PI3K-AKT signaling cascade, with NPs amplifying its toxicity.
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