Hepatotoxicity of paraquat on common carp (Cyprinus carpio L.)

Highlights: • Paraquat-exposure disturbs the metabolic destabilization of carp liver. • Paraquat has hepatotoxicity on common carp. • ROS and RNS may play an important role in paraquat-induced inflammatory response. • Apoptosis is probably involved in paraquat hepatotoxicity in carp. Paraquat (PQ) is a nonselective herbicide that is used worldwide and has been demonstrated to be a high risk to aquatic organisms. However, relatively little is known about the mechanisms on detoxification and hepatotoxicity of PQ in fish. In the present study, a sub-acute toxicity test of PQ exposure on common carp at 1.596 and 3.192 mg L^{− 1} for 7 d was conducted under laboratory conditions. The results showed that the transcriptional levels of cytochrome P450s (CYPs), such as CYP1A, CYP2K, and CYP3A138, GSTα and GSTpi, and export pump gene MDR1, as well as the erythromycin-N-demethylase (ERND) activity were generally up-regulated by PQ exposure for 7 d, indicating that these genes or enzymes are potentially involved in the detoxification of PQ in the fish liver. Further research showed that PQ exposure significantly increased the levels of HSP70, HSP90, NOS, and MDA; promoted expression of pro-inflammatory cytokines, including IL-6 and IL-8; altered the levels of anti-inflammatory cytokines IL-10 and TGF-β, and generally reduced the levels of T-AOC, SOD, CAT, and GSH. In addition, we also found that caspase-3, caspase-8, and caspase-9 were significantly activated in the fish liver following PQ exposure. In brief, the present study showed that PQ exposure induced fish liver injury by destabilizing the metabolism of fish, inhibiting antioxidant enzyme activity, elevating lipid peroxidation, and promoting an immune inflammatory response and apoptosis. The present study further enriches and perfects the mechanism theory of PQ hepatotoxicity to fish, which may be valuable for the risk assessment of PQ and human health protection.