Benzo[a]pyrene exposure increases inflammation, lipid accumulation, and lipid metabolism disfunction in the clam Ruditapes philippinarum.

Environmental pollution influences human diseases like metabolic dysfunction associated fatty liver disease (MAFLD). Bivalves' digestive glands are confronted with persistent organic pollutants (POPs) pollution, resulting in lipid metabolism disorders, and this process is also similar to the formation of MAFLD. In this study, we chose benzo[a]pyrene (B[a]P), a typical POPs, to investigate the impaired lipid metabolism and inflammatory risk of digestive glands in clam Ruditapes philippinarum towards B[a]P. The results indicated that accumulation of B[a]P in digestive glands was progressively higher and consistent with changes in lipid content. B[a]P induced impaired lipid metabolism of clam digestive glands through the endoplasmic reticulum stress pathway. We also identified signaling pathways that regulate lipid metabolism. B[a]P induced NF-kB through cellular stress, lipotoxicity, metabolic and immune pathways, causing metabolic inflammation, while the TGF-β pathway exerts anti-inflammatory effects. Our findings in clam aim to be useful for understanding how B[a]P impacts human MAFLD progression.