Due to overuse and terrestrial input, there are large quantities of
phoxim and
prometryne residues in some aquatic environments. In the present study, the effects of these compounds on Penaeus vannamei hepatopancreas were analysed at the transcriptome level to investigate toxicity in this nontarget aquaculture organism. Twelve normalised cDNA libraries were constructed using
RNA from
phoxim and
prometryne treatment groups, and an untreated control group. A total of 667,750,902 clean reads were obtained. Analysis of differentially expressed genes (DEGs) identified 449 in control vs
phoxim groups, 185 in control vs
prometryne groups, and 183 in
prometryne vs
phoxim groups. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis,
arachidonic acid metabolism, pancreatic secretion,
linoleic acid metabolism, and
beta-alanine metabolism pathways were significantly enriched in control vs
phoxim groups. In control vs
prometryne groups, lysosome,
pentose and
glucuronate interconversion, antigen processing and presentation, and
glycosaminoglycan degradation pathways were significantly enriched. In
prometryne vs
phoxim groups, protein digestion and absorption, extracellular matrix (ECM)-receptor interaction, PI3K-Akt signalling,
cell adhesion molecule (CAM), AGE-RAGE signalling related to
diabetic complications, focal adhesion, and
renin secretion pathways were significantly enriched. In further detailed analysis,
glutathione S-transferase (GST),
glutathione peroxidase and basic
phospholipase A2 were downregulated in the
phoxim treatment group, indicating that
phoxim damaged hepatopancreas. Upregulation of
phospholipase A2 (secretory phospholipase A2-like) indicates possible inflammatory pathological injury to hepatopancreas caused by
phoxim. Meanwhile, downregulation of CD63 indicates that
prometryne affect the immune system.