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Cadmium (Cd) is a major pollutant in water, and long-term Cd exposure seriously threatens aquatic organisms. This study evaluated the effects of dietary Cd on growth performance, tissue Cd accumulation, oxidative stress, endoplasmic reticulum (ER) stress, inflammation, apoptosis, and anti-stress response in juvenile black seabream (Acanthopagrus schlegelii). Six experimental diets containing different concentration of Cd were formulated: 0.02 (Control, Cd0.02), 1.60 (Cd1.60), 24.29 (Cd24.29), 49.04 (Cd49.04), 117.26 (Cd 117.26), and 289.65 (Cd289.65) mg/kg. A feeding experiment was performed on 540 juvenile black seabreams (initial weight, 1.42 ± 0.01 g), which were conducted for ten weeks. The findings revealed that Cd in the diet lowered weight gain (WG) and specific growth rate (SGR), but had no effect on survival. Dramatically positive linear trends were found between increasing dietary Cd contents and tissue Cd accumulation, including liver, kidney, and muscle. Dietary Cd exposure increased malondialdehyde (MDA) production in both serum and liver, hence, caused oxidative stress. The endoplasmic reticulum (ER) stress-related genes, including grp78, atf6, and xbp1, were markedly increased with increased dietary Cd levels, showing ER stress was triggered. Likewise, transcriptional expression levels of genes related to anti-stress response mt2, hsp70, and hsp90 were linearly up-regulated with increased dietary Cd contents. Regarding apoptosis, the transcriptional expression levels of pro-apoptosis genes caspase7, caspase9, and bax and anti-apoptosis gene bcl-2 were all significantly promoted with the increasing dietary Cd levels. Similar patterns were found for gene expression levels linked to inflammatory response, as the dietary Cd contents increased, nuclear transcription factor nf-κb, pro-inflammatory cytokines tnfα and il-1β, and anti-inflammatory il-10 and tgfβ were dramatically elevated. In conclusion, dietary Cd supplementation suppressed growth performance, increased Cd deposition in tissues, induced oxidative stress, ER stress, apoptosis, and inflammation. In contrast, black seabream juveniles also showed substantial tolerance for dietary Cd exposure by promoting anti-stress ability.

As a functional fatty acid, Arachidonic acid (ARA) plays an important role in immunity due to its metabolites in mammals, which have been extensively studied in mammals. However, studies on the function of metabolites produced by dietary ARA in aquatic animals are not comprehensive and in-depth. Hence, an eight-week feeding trial was conducted to evaluated the regulatory effects of dietary ARA and its metabolites-eicosanoids on inflammation, oxidative stress and apoptosis in the liver of Acanthopagrus schlegelii with an initial weight of 0.99 ± 0.10 g. Six isonitrogenous and isolipidic (41% protein, 14% lipid) diets were formulated with gradient levels of ARA: 0% (ARA0.10), 0.5% (ARA0.59), 1.0% (ARA1.04), 1.5% (ARA1.42), 2.0% (ARA1.94), 2.5% (ARA2.42), respectively, and palmitic acid was used to regulate lipid levels. Results showed that the key enzyme contents of ARA metabolic pathway such as phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), lipoxygenase (LOX) cytochrome P450 (CYP450), prostaglandin E2 (PGE2), leukotriene C4 (LTC4) and 20-hydroxyeicosatetraenoic acid (20-HETE) in the liver were increased with dietary ARA levels increased. High levels of dietary ARA (1.94% and 2.42%) activated the gene expression levels of nuclear factor kappa B (nf-κb), which were confirmed by the results of immunofluorescence assay. Likewise, the expression levels of pro-inflammatory cytokines (tnf-α and il-1β) were up-regulated by ARA1.94 and ARA2.42 groups. Fish fed with excess ARA level has significantly low antioxidant capacity by decreasing the activity of related antioxidant parameters and down-regulating the expression level of related genes. The pro-apoptotic related genes (bax and caspase 7/9) were markedly up-regulated as dietary ARA levels increased from 1.04% to 2.42%. Collectively, excess dietary ARA levels (1.92% and 2.42%) produced excess eicosanoids, triggering inflammation via activating NF-κB expression and promoting its nuclear translocation, resulting in oxidative stress by reducing antioxidant parameters (SOD, GSH and GPX), inducing cell apoptosis through up-regulating pro-apoptotic gene expression levels.

An eight weeks feeding trial was conducted to evaluate the potential of cottonseed oil (CSO) as a substitute for fish oil (FO) on juvenile black seabream (Acanthopagrus schlegelii) (2.29 ± 0.01 g). Five diets were formulated with pure FO (FO) or partial CSO replacement of FO: 20% CSO (CSO20), 40% CSO (CSO40), 60% CSO (CSO60) and 80% CSO (CSO80), respectively. Results showed that fish fed CSO60 diet significantly increased growth performance compared to control group. Hepatic expression of genes related to long-chain polyunsaturated fatty acid biosynthesis were significantly up-regulated by dietary CSO60 compared to FO group. Hepatic paraffin section and serum biochemical indices showed that fish fed dietary CSO80 could increase vacuolar fat drops and cause liver damage. The expression levels of peroxisome proliferators-activated receptor alpha and its downstream lipolysis related genes were markedly up-regulated with the increasing of replacement levels of CSO, opposite results were recorded in sterol regulatory element-binding protein-1c and lipogenesis related genes. The malondialdehyde content in liver was decreased with the increasing replacement levels of CSO, whereas the antioxidant parameters were significantly higher in CSO60 group compared to FO group. Phosphatidylinositol-3 kinase and protein kinase B expression levels were significantly up-regulated by dietary CSO80, triggering inflammation by activating nuclear factor kappa b. Dietary CSO60 dramatically promote target of rapamycin expression level. With the increasing replacement levels of FO by CSO, the expression level of ribosomal protein S6 kinase 1 was significantly increased, whereas opposite result was found for the eukaryotic translation initiation factor 4E binding protein 2. Collectively, based on weight gain, double broken line model analysis showed that a maximum growth occurred at 59.13% replacement of dietary FO by CSO. These findings demonstrate that dietary CSO60 can improve growth and antioxidant capacity. However, dietary CSO80 can result in lipid deposition, liver injury and inflammation, hence, suppress growth performance.

Cholesterol, which acts as a substrate for the synthesis of ovarian sex hormones, could promote ovarian development. However, crustaceans cannot synthesize cholesterol and must obtain it from diet for growth, molt and gonadal development. Three isonitrogenous and isolipidic diets were formulated to contain 0.12%, 1.00% and 2.50% cholesterol, respectively. The results showed that dietary 1.00% and 2.50% cholesterol significantly increased percent weight gain (PWG) and specific growth rate (SGR), moreover, crabs fed diet with 1.00% cholesterol had the highest gonadosomatic index (GSI) among all treatments. Cholesterol (CHO) and triglyceride (TG) concentrations in tissues significantly increased with dietary cholesterol levels increasing from 0.12% to and 2.50%. Targeted metabolomics analyses indicated that crabs fed 1.00% cholesterol diet exhibited higher steroid hormones, such as progesterone, pregnenolone, estrone, estradiol and estriol than those fed the other diets. In addition, crabs fed the 1.00% cholesterol diet significantly up-regulated the expression of genes related to cholesterol transport, steroid hormone synthesis and ovarian development in hepatopancreas and ovary. Transcriptomics analyses revealed that DEGs (differentially expressed genes) in crabs fed 1.00% cholesterol diet were associated with “metabolism of xenobiotics by cytochrome P450″ and “progesterone-mediated oocyte maturation”. In conclusion, the results of present study demonstrated that dietary 1.00% cholesterol promoted growth and ovarian development by improving the cholesterol transport and steroid hormone synthesis for female swimming crabs.

An eight-week feeding trial was conducted to investigate the effects of dietary lipid sources on growth performance, fatty acids composition in tissue and expression of genes related to lipid metabolism in juvenile largemouth bass (Micropterus salmoides). Four experimental diets were formulated to contain 6% coconut oil (CO), rapeseed oil (RO), linseed oil (LO) and fish oil (FO), respectively. Each diet was fed to triplicate groups of juvenile for 8 weeks. The results indicated that final body weight (FBW), percent weight gain (PWG), specific growth rate (SGR), feed efficiency (FE), survival, hepatopancreas index (HSI), viscerosomatic index (VSI) and intraperitoneal fat ratio (IPF) were not significantly influenced by dietary different lipid sources (P＞0.05). Moreover, proximate composition in whole body, dorsal muscle and liver were also not significantly affected by dietary different lipid sources (P ＞0.05). Fish fed with FO diet was significantly higher MDA concentration in hepatic and serum than those fed with CO, RO and LO diets (P