Polystyrene microplastics induced inflammation with activating the TLR2 signal by excessive accumulation of ROS in hepatopancreas of carp (Cyprinus carpio)

Polystyrene microplastics (PS-MPs) affect the immune defense function on carp (Cyprinus carpio). The PS-MPs model of carp was established by feeding with PS-MPs particle size of 8 mu m and concentration of 1000 ng/L water. Hepatopancreas function test revealed the activities of AKP, ALT, AST and LDH abnormal increase. PS -MPs induced tissue damage and lead to abnormal hepatopancreas function. The PS-MPs also induced a oxida-tive stress with the antioxidant enzymes SOD, CAT, GSH-PX, and T-AOC activities decreasing and reactive ox-ygen species (ROS) excessive accumulation. PS-MPs activated the Toll like receptor-2 (TLR2) signaling pathway. The mRNA and protein expressions of TLR2, Myeloid differentiation primary response 88 (MyD88), tumor ne-crosis factor receptor-associated factor 6 (TRAF6), NF-kappa B p65, Tumor necrosis factor (TNF-alpha), Interleukin-1 beta (IL-1 beta), Inducible Nitric Oxide Synthase (iNOS), and cycooxygenase 2(COX2) was revealed increased in both hepatopancreas and hepatocytes with the qPCR and Western blotting analysis mode. ELISA showed the ex-pressions of TNF-alpha, IL-1 beta, iNOS, and COX2 inflammatory molecule were increased in both hepatopancreas and hepatocytes. The results showed that PS-MPs caused a serious injure in the hepatopancreas and brought serious effects on the inflammatory response of carp. The present study displayed the harm caused by PS-MPs in freshwater fish, and provided some suggestions and references for toxicological studies of microplastics in freshwater environment.

Automated summary

By feeding carp with polystyrene microplastics (PS-MPs) particles of 8 μm in size and a concentration of 1000 ng/L water, a PS-MPs model of carp was established. An abnormal increase in the activities of AKP, ALT, AST, and LDH in the hepatopancreas indicated damage to this organ's function caused by PS-MPs. PS-MPs also induced oxidative stress, with a decrease in the activities of antioxidant enzymes and excessive accumulation of reactive oxygen species. Furthermore, PS-MPs activated the Toll-like receptor-2 (TLR2) signaling pathway, leading to increased expression of inflammatory molecules in both hepatopancreas and hepatocytes.