NOD-like receptor signaling pathway activation: A potential mechanism underlying negative effects of benzo(α)pyrene on zebrafish.

Benzo(α)pyrene (BaP) is one of typical polycyclic aromatic hydrocarbons (PAHs) in aquatic environments and has been shown to cause toxic effects to aquatic animals. Although the negative effects of BaP have been investigated, the potential toxic mechanisms remain uncharacterized. To explore the potential mechanisms mediating the toxic effects of BaP, zebrafish (Danio rerio) were exposed to BaP for 15 days and the toxic effects of BaP in zebrafish liver were investigated using physiological and transcriptomic analyses. After 15-day BaP exposure, zebrafish liver exhibited abnormalities including increased cytoplasmic vacuolation, inflammatory cell infiltration, swelled nuclei and irregular pigmentation. BaP exposure also induced oxidative stress to the liver of zebrafish. Transcriptomic profiles revealed 5129 differentially expressed genes (DEGs) after 15-days of BaP exposure, and the vast majority of DEGs were up-regulated under BaP treatment. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses suggest that genes related to immune response were significantly dysregulated. Furthermore, the nucleotide-binding, oligomerization domain (NOD)-like receptor signaling pathway was significantly enriched and most of the genes in this pathway exhibited enhanced expression after BaP exposure. These results partially explained the mechanisms underlying the toxic effects of BaP on zebrafish liver. In conclusion, BaP has the potential to induce physiological responses in zebrafish liver through altering associated genes.