Two genes related to apoptosis in the hepatopancreas of juvenile prawn, Macrobrachium nipponense: Molecular characterization and transcriptional response to nanoplastic exposure

Nanoplastics have been widely found in the global water environment, causing plastic pollution and affecting human beings and numerous organisms. Studies involving freshwater crustacean exposure to nanoplastics, however, are limited. In this study, juvenile prawns (Macrobrachium nipponense) were exposed to 75 nm polystyrene nanoplastics at different concentrations (0, 5, 10, 20, or 40 mg/L) for a 28-d chronic exposure experiment. To study the effects of exposure to nanoplastics on hepatopancreas cell apoptosis, C-Jun N-terminal kinase (JNK) and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA) genes were selected, and hepatotoxic enzyme activities and Toll pathway- and apoptosis-related gene expression were determined. For the first time, full-length Mn-JNK and Mn-PIK3CA cDNAs were cloned from M. nipponense. Homologous comparisons showed that JNK and PIK3CA had conserved functional sequences. The apoptosis rate in the high-concentration nanoplastic group (40 mg/L) was significantly higher than in the low-concentration nanoplastic (5 mg/L) and control groups (0 mg/L). The alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamyl transpeptidase (GGT) and xanthine oxidase (XOD) enzyme activities in the hepatopancreas increased with exposure to higher concentrations of nanoplastics. In addition, the levels of apoptosis- and Toll pathway-related gene expression and JNK and PIK3CA gene expression were initially increased, then decreased with exposure to higher concentrations of nanoplastics. This study showed that polystyrene nanoplastics activate toll-related pathways leading to apoptosis and hepatopancreas damage, which provides theoretical support for future aquatic toxicological research.