Tire wear particle leachate induces lipid metabolism disorders in Procambarus clarkii, leading to liver inflammation and mitochondrial dysfunction in hepatocytes

Tire wear particle (TWP) leachate, an emerging pollutant that has gained widespread attention in recent years, poses a serious threat to aquatic ecosystems and particularly to economically important freshwater species. The toxicity of TWP leachate to aquatic organisms underscores its detrimental impact on these ecosystems. In this study, the crayfish Procambarus clarkii was exposed to TWPs at concentrations of 0 %, 0.5 %, 5 %, and 40 %, with normal feeding provided daily for 28 days. With increasing TWP leachate concentrations, the neutral lipid content in the P. clarkii liver tissue increased significantly, cell necrosis intensified, and tissue lesions became more severe. At the mRNA level, the Gene Ontology (GO) analysis indicated the enrichment of oxidoreductase activity, apoptotic cell recognition, and autophagosome organization, while pathways associated amino acid metabolism, lipid metabolism, glycan biosynthesis and metabolism, and carbohydrate metabolism were activated. These processes resulted in lipid metabolism disorders, mitochondrial dysfunction in hepatocytes, and the induction of liver inflammation and apoptosis. Under medium- to high-TWP leachate exposure, the activities of glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) in P. clarkii livers were significantly reduced, impairing the organ's antioxidant capacity. These findings highlight the biological toxicity of TWP leachate to P. clarkii and provide new reference data for future environmental management strategies addressing TWP pollution.