Pyraclostrobin (PYR), a strobilurin fungicide, has been widely used to control fungal diseases, posing potential risk to aquatic organisms. However, the toxic effects of PYR to fish remained largely unknown. In this study, common carp (Cyprinus carpio L.) was exposed to environmentally relevant levels of PYR (0, 0.5 and 5.0 μg/L) for 30 days to assess its chronic toxicity and potential toxicity mechanism. The results showed that long-term exposure to PYR induced hepatopancreas damage as evident by increased in serum transaminase activities (AST and ALT). Moreover, PYR exposure remarkably enhanced the expressions of hsp70 and hsp90, decreased the levels of antioxidant enzymes and biomarkers and promoted the reactive oxygen species (H2O2 and O2-) and MDA contents in carp hepatopancreas. PYR exposure also upregulated apoptosis-related genes (bax, apaf-1, caspase-3 and caspase-9) and reduced anti-apoptosis gene bcl-2 in fish hepatopancreas. Moreover, PYR exposure altered the expressions of inflammatory cytokines (IL-1β, IL-6, TNF-α and TGF-β) in the serum and hepatopancreas and the level of NF-κB p65 in the hepatopancreas. Further research indicated that PYR exposure markedly changed the levels of immune parameters (LYZ, C3, IgM, ACP and AKP) in the serum and/or hepatopancreas, indicating that chronic PYR exposure also has immunotoxicity on fish. Additionally, we found that PYR exposure upregulated p38 and jnk MAPK transcription levels, suggesting that MAPK may be play important role in PYR-induced apoptosis and inflammatory response in the hepatopancreas of common carp. In summary, PYR exposure induced oxidative stress, triggered apoptosis, inflammatory and immune response in common carp, which can help to elucidate the possible toxicity mechanism of PYR in fish.
Keywords: Apoptosis; Common carp; Hepatopancreas toxicity; Immunotoxicity; Oxidative stress; Pyraclostrobin.
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