Revelation of benzo(a)pyrene-induced latent toxicity mechanism to intestinal histomorphology and oxidative status for common carp (Cyprinus carpio) through transcriptional and single-cell sequencing

Common carp (Cyprinus carpio) (mean weight 50.0 ± 10.0 g) were exposed for 15 d with benzo[a]pyrene (B[a]P) concentrations of 0, 2.5 and 25 μg/kg in the water. For markers of oxidative stress, intestinal contents of glutathione (GSH) and malondialdehyde and activities of catalase and superoxide dismutase were significantly elevated after 15-d B[a]P exposure. For intestinal histology and ultrastructure analysis, intestinal histiocytes not only swelled, but also intensified blood aggregation, resulting in hematoma after exposed to high B[a]P concentration. For intestinal transcriptome response, GSH signaling pathway was abnormally activated after exposure to B[a]P, thereby resulting in intestinal oxidative damage. Meanwhile, exposure to B[a]P suppressed intestinal platelet activation depending on ADP signaling pathway. Exposure to high B[a]P concentration induced intestinal cellular edema through the suppression of Lysosome-Phagosome pathway. For scRNA-seq results, myeloid cells under B[a]P stress, despite having evolved into cell types with distinct specialties, still retained innate immune functions such as Macrophage_3. The present study provides valuable and front-edged insights for developing sustainable solutions to address the challenges posed by PAHs waste and B[a]P contamination on aquaculture system. [Display omitted] •B[a]P induced common carp intestinal histomorphology and oxidative damage.•Exposure to B[a]P caused intestinal oxidative damage by GSH signaling pathway.•B[a]P stress suppressed intestinal platelet activation through ADP signaling pathway.•B[a]P exposure trigger intestinal pathologic edema via Lysosome-Phagosome pathway.