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Microplastics and bisphenol A exposure induce hepatopancreatic damage and lipid metabolism disorders in Portunus trituberculatus
Summary
This study exposed female swimming crabs (Portunus trituberculatus) to microplastics and bisphenol A individually and in combination, finding that both pollutants caused hepatopancreatic damage and lipid metabolism disruption via distinct but overlapping mechanisms. Combined exposure produced additive harm to liver-like tissue and metabolic function.
This study exposed female Portunus trituberculatus crabs (developmental stages III-IV) to microplastics (MPs) and bisphenol A (BPA) individually or combined for 21 days. Assessments included growth, histology, enzyme/gene expression, and metabolomics. Both MPs and BPA caused hepatopancreatic damage and lipid accumulation but via distinct mechanisms. MPs groups showed downregulated acetyl-CoA carboxylase (ACC) gene expression and upregulated fatty acid transport protein (FATP) genes, with reduced N-acetyl-d-glucosamine synthesis, suggesting disrupted energy metabolism (e.g., nucleotide sugar synthesis and ABC transport). BPA groups showed similarly downregulated ACC but upregulated FATP and Fatty Acid-Binding Protein (FABP) genes. Metabolomic shifts included decreased uric acid/prostaglandin F2α and increased glycochenodeoxycholic acid/inositol-1,3-bisphosphate, indicating estrogenic effects and hormonal imbalance. Combined exposure exacerbates hepatopancreatic injury and lipid metabolism disorders through complex mechanisms of action, highlighting heightened risks to aquatic ecosystems and potential human health impacts. The study underscores MPs and BPA as dual threats with unique and compounded toxicity pathways.
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