Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)

Abstract

Microplastics (MPs) are a serious threat to the living environment of aquatic organisms. However, there are fewer studies on the toxicity of microplastics to freshwater organisms. This study aimed to establish a polystyrene microplastics (PS-MPs) model by feeding carp (Cyprinus carpio) PS-MP (1000 ng/L) particles 8 μm in size. HE staining revealed a mass of inflammatory cells infiltrated in the carp hepatopancreas. The activities of alkaline phosphatase (AKP), aspartate transaminase (AST), lactate dehydrogenase (LDH), and alanine transaminase (ALT) were strengthened considerably, suggesting that PS-MPs cause injury to the hepatopancreas of carp. Real-Time polymerase chain reaction and western blotting results indicated increased levels of glucose-regulated protein 78 (GRP78), (PKR)-like ER kinase (PERK), eukaryotic translation initiation Factor 2α (EIF2α) and activating transcription Factor 4 (ATF4) genes and increased levels of inflammatory factors downstream of endoplasmic reticulum stress (ERs) thioredoxin-interacting protein (TXNIP), NOD-like receptor protein 3 (NLRP3), interleukin-18 (IL-18), interleukin-1β (IL-1β), and caspase 1. Increased expression of microtubule-associated protein-2 (LC3II), autophagy-related 5 (ATG5) and autophagy-related 12 (ATG12) genes revealed that PS-MPs promoted autophagy in carp hepatocytes. The enhanced expression of the Caspase 12, Caspase 3, and Bax genes suggested that PS-MPs led to the apoptosis of carp hepatocytes. These results suggest that PS-MPs result in serious injury to the hepatopancreas of carp. The present study of PS-MPs in freshwater fish from the aspect of endoplasmic reticulum stress was conducted to provide references and suggestions for toxicological studies of PS-MPs in freshwater environments.