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Bisphenol A (BPA), as a phenolic compound, is harmful to human health, and its residue in the aquatic environment also threatens the health of aquatic animals. In this research, the toxicity effects of BPA on liver tissues were evaluated in common carp (Cyprinus carpio) after long-term exposure. Fish were exposed to five concentrations of BPA (0, 0.01, 0.1, 0.5 and 2 mg/L) for 30 days. The blood and liver tissues were gathered to analyze biochemical indices and genes transcription levels. The data related to lipid metabolism showed that BPA exposure increased serum total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) levels, upregulated the expressions of fatp1, pparγ, fas, atgl, hsl, pparα, cpt1b, acox-1, and downregulated the expression of dgat1 in liver. Antioxidative parameters displayed a reduced antioxidant ability and increased lipid peroxidation after BPA exposure. Meanwhile, the upregulations of nrf2, ho-1, cyp1a and cyp1b genes revealed an adaptive response mechanism against oxidative stress-induced adverse effects. After 30 days of exposure, BPA induced apoptosis and endoplasmic reticulum stress (ERS) via upregulating the expression levels of apoptosis and ERS-related genes and increasing Ca 2+ concentration in liver. Moreover, the downregulation of mtor and the upregulation of atg3, atg7, tfeb, uvrag and mcoln1 indicated that BPA could influence the normal process of autophagy. Furthermore, BPA exposure activated toll like receptors (TLRs) pathway to mediate the inflammatory response. Our results demonstrated that BPA exposure disturbed lipid metabolism, and induced oxidative stress, ERS, apoptosis, autophagy and inflammatory response in the liver of common carp. These findings contributed to the understanding of hepatotoxicity mechanism induced by BPA in fish., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Baicalin, a main bioactive compound of Scutellaria baicalensis, has a variety of pharmacological activities including antioxidation, anti-inflammation and hepatoprotection. However, there are few reports on these biological activities in fish. Therefore, the aim of this study was to assess the effects of baicalin on growth performance, antioxidative status and hepatoprotection in tilapia. The fish were fed on different doses of baicalin (0, 0.4, 0.8 and 1.6 g/kg diet). After feeding 60 days, parts of fishes were netted, and the blood, liver, gills and muscle tissues were collected to analyze the antioxidative effect. The remaining fishes were injected with saline or hydrogen peroxide (H 2 O 2 ) for challenge test. The results showed that the specific growth rate of fish was slightly increased in three baicalin treatments, and the feed efficiency was clearly improved in 0.4 g/kg baicalin treatment. Meanwhile, the antioxidative capacity in blood, liver and/or gill was enhanced in treatments with 0.4, 0.8 and/or 1.6 g/kg baicalin. After challenge test, the pre-treatments with baicalin effectively alleviated H 2 O 2 -induced liver injury. In serum and liver, pre-treatments with 0.8 and/or 1.6 g/kg baicalin suppressed the oxidative damage induced by H 2 O 2 , as evidenced by improvement of the levels of SOD, T-AOC and GSH and the decline of MDA level. More important, pre-treatments with 0.4, 0.8 and/or 1.6 g/kg baicalin blocked the upregulation of mRNA levels of tlr1, myd88, irak4, rela, tnf-α and il-1β in H 2 O 2 -induced liver injury. In summary, dietary baicalin supplementation could improve feed efficiency, enhance antioxidative ability and alleviate oxidative stress-induced hepatotoxicity in tilapia., (Copyright © 2020. Published by Elsevier Inc.)

Resveratrol, a dietary polyphenol, has been shown to exert antioxidation, hepatoprotection, anti-inflammation and immunostimulation. However, the effects and underlying mechanism of resveratrol on liver injury in fish are still unclear. In the present study, we investigated the potential protective effects and mechanism of resveratrol on oxidative stress-induced liver damage in tilapia. Fish were fed diet containing four doses of resveratrol (0, 0.1, 0.3, and 0.6 g/kg diet) for 60 days, and then given an intraperitoneal injection of H 2 O 2 or saline. The results showed that administration of resveratrol significantly ameliorated H 2 O 2 -induced liver injury. In serum and liver, resveratrol treatment suppressed the oxidative stress, as evidenced by the decline of lipid peroxidation level and increase of antioxidant activity. Resveratrol also activated erythroid 2-related factor 2 (Nrf2) signaling pathway and enhanced the heme oxygenase 1 (HO-1), NAD(P) H:quinone oxidoreductase 1 (NQO-1), glutathione S-transferase (GST) mRNA levels. Meanwhile, resveratrol treatment repressed TLR2-Myd88-NF-κB signaling pathway to decrease the inflammatory response in H 2 O 2 -induced liver injury as evidenced by the lower interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-8 mRNA levels and higher IL-10 mRNA level. Moreover, resveratrol treatment attenuated immunotoxicity in liver of H 2 O 2 -treated fish, accompanied by upregulation of hepcidin (HEP), complement 3 (C3) and lysozyme (LZM) mRNA levels. Overall results suggested that the protection of resveratrol on H 2 O 2 -induced liver injury, inflammation and immunotoxicity was due to its antioxidant property and its ability to modulate the Nrf2 and TLR2-Myd88-NF-κB signaling pathways., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The aim of the present study was to investigate the protective effects of Ganoderma lucidum polysaccharide (GLPS) against carbon tetrachloride (CCl 4 )-induced hepatotoxicity in vitro in common carp. Precision-cut liver slices (PCLSs), which closely resemble the organ from which they are derived, were employed as an in vitro model system. GLPS (0.1, 0.3, and 0.6 mg/ml) was added to PCLS culture system before the exposure to 12 mM CCl 4 . The supernatants and slices were collected to detect molecular and biochemical responses to CCl 4 and PCLS treatments. The levels of CYP1A, CYP3A, and CYP2E1 were measured by ELISA; the mRNA expressions of TNF-α, IL-1β, IL-6, and iNOS were determined by RT-PCR; and the relative protein expressions of c-Rel and p65 were analyzed by western blotting. Results showed that GLPS inhibited the elevations of the marker enzymes (GOT, GPT, LDH) and MDA induced by CCl 4 ; it also enhanced the suppressed activity of antioxidant enzymes (SOD, CAT, GSH-Px, T-AOC). The treatment with GLPS resulted in significant downregulation of NF-κB and inflammatory cytokine mRNA levels and significant decreases in the hepatic protein levels of CYP1A, CYP3A, and CYP2E1. These results suggest that GLPS can protect CCl 4 -induced PCLS injury through inhibiting lipid peroxidation, elevating antioxidant enzyme activity, and suppressing immune inflammatory response.

The protective effects of Lycium barbarum polysaccharides (LBPs) against carbon tetrachloride-induced hepatotoxicity in common carp were investigated in vitro and in vivo. Precision-cut liver slices (PCLSs) were employed as an in vitro model system. LBPs (0.1, 0.3 and 0.6 mg/ml) was added to PCLSs culture system before (pre-treatment), after (post-treatment) and both before and after (pre- and post-treatment) the exposure of PCLSs to 12 mM CCl4. The supernatants and PCLSs were collected for biochemical analyses. Results showed that LBPs inhibited the elevations of the marker enzymes (GOT, GPT, LDH and AKP) and MDA induced by CCl4 in all LBPs treatments and it also enhanced the suppressed antioxidant enzymes (SOD, CAT, GSH-Px, GST) and GSH, in the pre-treatment and pre- and post-treatment. In vivo, fish were fed diets containing LBPs at 0.1, 0.5 and 1% for 60 d before an intraperitoneal injection of 30% CCl4 in olive oil at a volume of 0.05 ml/10 g body weight. At 72 h post-injection, blood and liver samples were taken for biochemical analyses. Results showed that LBPs at 0.5 and 1% significantly reduced the levels of GOT, GPT and LDH in the serum; the decreases of the antioxidant enzymes and the increase of MDA in the liver tissue were inhibited markedly. Moreover, LBPs even at lower concentration exerted a potent DPPH scavenging activity. Overall results prove the hepatoprotective and antioxidant effects of LBPs and support the use of LBPs as a hepatoprotective agent in fish., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Cyclophosphamide (CTX) is a common immunosuppressant, and it can also results in liver injury in human and animals. In this study, the CTX-induced liver injury mechanism in tilapia (Oreochromis niloticus) was investigated by studying alteration of endoplasmic reticulum stress (ERS), inflammation and anti-oxidative status. Tilapia was intraperitoneally injected CTX at the doses of 10, 25, 50, 75 and 100 mg·kg−1, and the blood and liver tissues were collected. The results showed that CTX administration had a significant cytotoxicity on hepatocytes, and increased the liver index. The extensive vacuolar degeneration, unclear cell outline and other histological lesions were also observed. CTX administration markedly decreased the antioxidant ability and enhanced lipid peroxidation in liver. Furthermore, qPCR data showed that CTX administration at 50–100 mg·kg−1 up-regulated gene expressions of cyp1a , cyp2k1 and cyp3a , and inflammatory response-related genes including rel , relb , nfκb1 , il-6 , il-8 , il-10 and tnf-α. CTX significantly promoted the mRNA levels of ERS-related genes (eif2α , crt , parp1 , grp78 , ire1 , xbp1s and chop) in a dose dependent manner. Additionally, CTX injection at 75–100 mg·kg−1 could down-regulate gene expressions of anti-oxidative status including nrf2 , ucp2 , ho-1 , gpx3 , gstα and cat. Overall results suggested CTX injection induced liver damage which was related to the cytotoxic effect on hepatocytes, decrease of antioxidant capacity, inflammatory response and ERS. [Display omitted] • CTX treatment induces hepatic injury in Nile tilapia. • CTX treatment inhibits antioxidant capacity. • CTX treatment stimulates inflammatory response. • CTX treatment promotes endoplasmic reticulum stress. [ABSTRACT FROM AUTHOR]