Juvenile Yellow Catfish Pelteobagrus Fulvidraco Research Articles

Effects of three short-chain fatty acids on growth, intestinal microbiota composition, and ammonia tolerance of juvenile yellow catfish Pelteobagrus fulvidraco

The objective of this research was to examine how the growth, ammonia tolerance, and intestinal microbiota composition of juvenile yellow catfish are affected by dietary supplementation of isobutyric acid (IBA), isovaleric acid (IVA), and 2-methylbutyric acid (2-MBA). During the 8-week trial, four groups were fed the basal diet (Control), and the basal diet supplementation with 0.25% IBA, IVA and 2-MBA, respectively. The research shows that the yellow catfish in the IBA and 2-MBA groups had a higher weight gain rate and specific growth rate than the control group, but feed conversion ratio has the opposite trend. Dietary supplementation of IBA and 2-MBA can significantly improve digestive enzymes activities (α-amylase, lipase, and trypsin) in intestinal tract and blood health (serum albumin increased, alanine transaminase and aspartate transaminase decreased). The up-regulation of IGF-1, Myod, and MyoG gene mRNA expression levels occurred significantly in the muscle tissue of the IBA, IVA, and 2-MBA groups, but IL 1 and IL8 genes in intestinal tract were significantly down-regulated. Supplementation of IBA, IVA and 2-MBA significantly increased the relative abundance of Candidatus Arthromitus, while decreased the relative abundance of Achromobacter, most notably in IBA group. After 96-h ammonia stress, cumulative mortality in IBA group was the lowest. Supplementing the diet of yellow catfish with IBA or 2-MBA can enhance their growth, digestive enzyme activity, and blood health status. Additionally, IBA can improve ammonia tolerance, which may be related to the increase abundance of Candidatus Arthromitus in intestine.

Effects of dietary sodium acetate on growth, intestinal microbiota composition, and ammonia tolerance of juvenile yellow catfish Pelteobagrus fulvidraco

Short-chain fatty acids (SCFAs), such as acetates, play a role in modifying metabolic disorders and regulating the homeostasis of the organism. In this study, the impact of dietary sodium acetate (SA) on growth, intestinal microbiota composition, and ammonia tolerance of yellow catfish. During a 56-day study, four groups of yellow catfish weighing an average of 2.72 ± 0.11 g were provided with diets containing varying proportions of SA. The diets included 0%, 0.1%, 0.2%, and 0.4% SA. Each batch consisted of three replicates, with each replicate containing 40 fish. The results indicated that dietary supplemented with 0.2% SA had significantly higher weight gain and specific growth rates than those in 0% and 0.1% groups. The feed efficiency ratio in 0% groups was significantly the highest. Dietary SA can significantly increase the activities of intestinal lipase, amylase, and pepsin, and the contents of liver total protein, immunoglobulin M, and 50% hemolytic complement, while decreasing the contents of liver triglyceride, glucose, high-density lipoprotein cholesterol, aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor-α, interleukin-1, and interleukin-8, and the activities of liver superoxide dismutase, and catalase. In addition, dietary SA significantly increased the relative abundance of beneficial bacteria (Achromobacter) and production of butyrate, meanwhile decreasing the harmful bacterial (Rhodobacter) abundance. After the challenge, cumulative mortality in fish fed 0% SA diets was higher than in fish fed 0.1–0.5% SA diets after 96 h ammonia stress. Correlation analysis showed that the SA induced the enhancement of the metabolic efficiency of carbohydrates, amino acids, and lipids were also associated with the increased relative abundance of Achromobacter. In general, SA can function as a beneficial additive for enhancing growth, intestinal health, and ammonia tolerance in yellow catfish.

Effects of ammonia and roxithromycin exposure on skin mucus microbiota composition and immune response of juvenile yellow catfish Pelteobagrus fulvidraco

As an inevitable factor in aquaculture, ammonia plays a critical role in macrolide antibiotic resistance, leading to accumulating of antibiotic-resistant bacteria in fish skin mucus. In this study, four experimental groups were implemented to test the effects of ammonia alone or in combination with roxithromycin for 28 days on skin mucus microbial composition and the immune response of yellow catfish: CON (control), AN (50.00 mg L−1 total ammonia nitrogen, TA-N), ROX (100 μg L−1 roxithromycin), and HR (50.00 mg L−1 TA-N, 100 μg L−1 ROX). This study demonstrated that ammonia or roxithromycin exposure resulted in increased plasma ammonia content and decreased total antioxidant capacity. Compared with AN group, the combined exposure of ammonia and roxithromycin inhibited the skin mucus immune response. Microbial composition analysis showed that combined exposure of ammonia and roxithromycin had no significant effect on skin mucus α-diversity as compared with CON group. The abundance of Cetobacterium, Rhizobiales_Incertae_Sedis_uncultured and Acinetobacter was increased significantly with the combined effect of ammonia and roxithromycin, these bacteria may be potentially antibiotic-resistant. As compared with CON group, the combined exposure of ammonia and roxithromycin did not affect skin goblet cell counts. This study suggests that combined exposure to ammonia and ROX increases the risk of the emergence of antibiotic-resistant bacteria.

Effects of dietary leucine on growth, antioxidant capacity, immune response, and inflammation in juvenile yellow catfish Pelteobagrus fulvidraco.

The experiment was conducted to investigate the effects of dietary leucine on growth, antioxidant capacity, immune response, and inflammation in juvenile yellow catfish. Five diets were formulated to contain five dietary leucine levels: 12.00 (control), 19.00, 26.00, 33.00, and 40.00gkg-1. Each diet was randomly assigned to triplicate groups of 30 juvenile fish (5.02 ± 0.15g) twice daily to apparent satiation for 56days. Weight gain rate, specific growth rate, and activities of liver superoxide dismutase, glutathione peroxidase, and serum lysozyme, as well as immunoglobulin M content, significantly increased with increase in dietary leucine levels up to 26.00gkg-1, but those values decreased significantly with a further increase in dietary leucine. On the contrary, the lowest malondialdehyde content was found in 26.00 and 33.00gkg-1 leucine groups. The expression levels of IGF 1 and MYF 5 genes in muscle were significantly upregulated with increase in dietary leucine levels up to 26.00gkg-1, but the expression of MSTN level showed the opposite trend. The lowest expression levels of IL 8 and TNFɑ genes in the liver were found in 26.00gkg-1 leucine groups. The quadratic regression analysis on weight gain, specific growth rate, and feed conversion ratio against dietary leucine levels indicated that the optimal dietary leucine requirement was estimated to be 26.84-27.00gkg-1of the dry diet.

Comparison of dietary arginine or/and inulin supplementation on growth, digestive ability and ammonia tolerance of juvenile yellow catfish Pelteobagrus fulvidraco

Most fish have limited use of arginine, and increasing arginine availability by adding other nutrients is an effective method. Inulin is thought to have potential synergistic effects with arginine. Four experiment groups were carried out to test the hypothesis that inulin can increase arginine availability of yellow catfish, including control, arginine, inulin and arginine mixed with inulin groups. The results showed that dietary arginine supplementation improved growth (weight gain and whole-body protein increased; IGF 1, MyoD, MyoG and Myf5 genes up-regulated), digestive ability (intestine protease and lipase increased), blood health (total protein and high-density lipoprotein cholesterol increased) and ammonia tolerance (cumulative mortality reduced; serum lysozyme, 50% hemolytic complement, respiratory burst and phagocytic indices increased) of yellow catfish, and reduced intestine inflammation (tumor necrosis factor and interleukin 1 decreased). Meanwhile, the addition of inulin to arginine-rich diets was further enhanced growth, digestive ability, intestine internal environment (butyric acid and total volatile fatty acids increased), blood health and ammonia tolerance (argininosuccinate synthetase, argininosuccinate lyase, arginase and ornithine transcarboxylase increased) of yellow catfish, and further relieved intestine inflammation. This study indicates that inulin can promote the utilization of dietary arginine; the potential synergistic effects between arginine and inulin were found in growth, digestive ability and ammonia tolerance of yellow catfish.

Chronic toxicity study of ammonia exposure in juvenile yellow catfish Pelteobagrus fulvidraco

In aquaculture systems, long-term low ammonia stress has not received enough attention because ambient ammonia easily does not reach lethal concentrations for fish. The purpose of this study was to investigate the growth performance of yellow catfish to chronic low ammonia exposure, and to clarify the growth tolerance upper limit (GTUL) for ammonia, which can help enterprises reduce costs. We measured the 56-d survival, growth and physiological status of yellow catfish (3.96 ± 0.05 g) reared in 0.00, 1.25, 2.50, 5.00 and 10.00 mg/L total ammonia nitrogen (TAN). The survival rate was significantly reduced at ammonia level up to 10.00 mg/L TAN. However, the weight gain rate, condition factor, feed intake, hepatosomatic index, serum acid phosphatase and immunoglobulin M contents, lysozyme activity, and Bcl2 expression were significantly decreased when ammonia level exceeded 1.25 mg/L TAN, while whole-body crude protein, muscle amino acids, serum ammonia, aspartate transaminase, liver tumor necrosis factor, interleukin 1 and 8 contents, and the expressions of GPX, TNFα, IL 8, P53, AKT, PTEN were significantly increased. We recommend that juvenile yellow catfish not be exposed to ammonia concentrations >1.25 mg/L TAN (0.026 mg/L NH3) for prolonged periods of time.

Effects of dietary cellulose supplementation on the intestinal health and ammonia tolerance in juvenile yellow catfish Pelteobagrus fulvidraco

Cellulose can reduce endogenous ammonia production of non-ruminant animals by altering intestinal microbiota structure. Although the utilization of cellulose in fish is limited, we speculate that cellulose has a potential role in regulating fish ammonia tolerance. Four experiment diets with different cellulose levels (Ctrl, 4.00%, 6.00% and 8.00%) were formulated and fed to yellow catfish for 84 days. This study found that dietary supplemented with 6.00% cellulose can improve growth performance (final body weight and weight gain rate), blood health (total protein, albumin and globulin), intestinal digestive enzyme activity (protease, lipase and cellulase), and ensure intestinal structure integrity (villi length), and maintain intestinal microbiota stability (Shannon and Chao1 indexes). After 96 h ammonia stress, serum ammonia content and cumulative mortality were negative correlated with Cetobacterium abundance. The activities of ammonia metabolism enzyme (glutamine synthetase, carbamyl phosphate synthetase, argininosuccinic acid synthase and arginase) and antioxidant enzyme (superoxide dismutase, catalase and glutathione peroxidase) in 4.00% and 6.00% cellulose groups were higher than those in Ctrl and 8.00% cellulose groups. The highest mRNA expression levels of antioxidant-related genes (Cu/Zn-SOD, CAT, GPX and GR) and inflammation-related genes (IL1, IL 8 and TNFɑ) were found in 8.00% cellulose group. This study indicates dietary supplemented with cellulose can increase the Cetobacterium abundance in intestinal tract, which is closely related to ammonia tolerance of yellow catfish. The levels of 4.00–6.00% cellulose in dietary is recommended in juvenile yellow catfish.

Fish Meal Replacement by Mixed Plant Protein in the Diets for Juvenile Yellow Catfish Pelteobagrus fulvidraco: Effects on Growth Performance and Health Status.

Increasing dietary replacement levels of fish meal by alternative plant proteins are of value for aquaculture. Here, a 10-week feeding experiment was undertaken to explore the effects of fish meal replacement by mixed plant protein (at a 2 : 3 ratio of cottonseed meal to rapeseed meal) on growth performance, oxidative and inflammatory responses, and mTOR pathway of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (2.38 ± 0.1 g, mean ± SEM) were randomly divided into 15 indoors fiberglass tanks, 30 fish each tank, and fed five isonitrogenous (44% crude protein) and isolipidic (9% crude fat) diets with fish meal replaced by mixed plant protein at 0% (the control), 10% (RM10), 20% (RM20), 30% (RM30), and 40% (RM40), respectively. Among five groups, fish fed the control, and RM10 diets tended to have higher growth performance, higher protein content, and lower lipid content in livers. Dietary mixed plant protein substitute increased hepatic free gossypol content and damaged liver histology and reduced the serum total essential amino acids, total nonessential amino acids, and total amino acid contents. Yellow catfish fed the control, and RM10 diets tended to have higher antioxidant capacity. Dietary mixed plant protein replacement tended to promote proinflammatory responses and inhibited mTOR pathway. Based on the second regression analysis of SGR against mixed plant protein substitutes, the optimal replacement level of fish meal by mixed plant protein was 8.7%.

Interactive effects of dietary zinc and water temperature on growth performance, Zn transport, heat shock response and lipid metabolism in the livers of juvenile yellow catfish Pelteobagrus fulvidraco

A better understanding of metabolic responses is necessary to elucidate interactive effects between water temperature and Zn. This study is performed to investigate the interactive influences of dietary Zn and water temperature on Zn transport, heat stress and lipid metabolism in the livers of freshwater teleost yellow catfish Pelteobagrus fulvidraco. A 2 × 2 factorial design is used in this study, which includes two levels of Zn at 38.5 and 131.2 mg Zn /kg diet for adequate- and high-Zn diets, and two levels of water temperature (28 and 32 °C). The feeding experiment continues for 7 weeks. Water temperature of 32 °C alleviates dietary Zn-induced reduction of growth performance and mRNA expression of znt2, znt10, zip11 and zip13, and abrogates dietary Zn-induced increment of mRNA expression of znt5 and znt8 of yellow catfish. Compared to dietary Zn addition, dietary Zn addition and water temperature of 32 °C increase hepatic Zn content and up-regulated mtf-1 mRNA expression. Compared to single dietary Zn addition, water temperature of 32 °C + dietary Zn addition increase mRNA expression of hsp70 and hsf1. Moreover, water temperature of 32 °C alleviates dietary Zn-induced reduction of TG content and acca mRNA expression, and abolishes the increment of mRNA expression of hsl and pparα induced by dietary Zn. Mechanistically, Zn regulates hsp90 by the MTF-1 binding to the hsp90 promoter. Thus, there is a significant interaction between dietary Zn and water temperature in affecting growth performance, Zn transport, heat shock responses and lipid metabolism. Our results also provide the innovative insights into the mechanism for the interaction between mineral elements and heat stress in fish. Statement of relevanceThe frequent heat waves and global warming influences the freshwater ecosystem, which in turn affects the growth performance, heat stress response, nutrient utilization and metabolism in fish. Our results provided the innovative insights into the interaction between mineral elements and heat stress in fish.

Insights into the mechanisms of tris(2-chloroethyl) phosphate-induced growth inhibition in juvenile yellow catfish Pelteobagrus fulvidraco.

With the gradual elimination of brominated flame retardants (BFRs), the production and application of tris (2-chloroethyl) phosphate (TCEP), as a substitute of BFRs, has increased greatly. The objective of the present study was to comprehensively explore the potential adverse effects of TCEP on fish growth and the possible underlying mechanisms. To this end, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP (0, 1, 10 and 100 µg/L) for 30 days. The results showed that exposure to high concentrations of TCEP (10 and 100 µg/L) significantly decreased body weight, body length and specific growth rate (SGR). Plasma IGF-I levels and hepatic mRNA levels of igf1 and igf1r were all reduced, while the transcriptional levels of IGFBPs (igfbp2, igfbp3, igfbp5) were significantly up-regulated in the liver of yellow catfish under exposure to 10 and 100 µg/L TCEP. TCEP-induced growth inhibition might be related to somatostatin (SS) signaling system, as evidenced by elevated mRNA transcriptions of ss in brain and its receptors (sstr2, sstr3, sstr5) in liver. In addition, fish exposed to high concentrations of TCEP displayed multiple histological alterations in liver. Taken together, these findings suggested that TCEP (>10 µg/L) might exert its inhibitory effect on fish growth through interfering with the GH/IGF axis and SS signaling system, and by impairing hepatic structures.

Effects of tris (2-chloroethyl) phosphate (TCEP) on survival, growth, histological changes and gene expressions in juvenile yellow catfish Pelteobagrus fulvidraco

Tris (2-chloroethyl) phosphate (TCEP) is an emerging aquatic environmental pollutant. In the present study, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP for 30 days. The results showed that TCEP exposure decreased the survival rate (100 μg/L), body weight (10 and 100 μg/L) and specific growth rate (10 and 100 μg/L) of juvenile yellow catfish. Exposure to TCEP resulted in pronounced damages of gill structures. Gene transcription analysis showed that the antioxidant capacity of the liver and gills was affected; CYP1A1 might contribute to phase I metabolism of TCEP in the liver rather than CYP1B1; TCEP stress might increase the demand of ion transport in fish gill; TCEP could stimulate the immune response and might induce apoptosis via a p53-Bax pathway and caspase-dependent pathway in gills. Collectively, these findings provide new insights into the toxic effects of TCEP on fish.

Effects of α-ethinyl estradiol (EE2) and diethylhexyl phthalate (DEHP) on growth performance, antioxidant status and immune response of juvenile yellow catfish Pelteobagrus fulvidraco

The four experimental groups were carried out to test the response of yellow catfish to EE2 and DEHP: control group was exposed to DMSO; EE2 group was exposed to 1.0 μg/L EE2; DEHP group was exposed to 1.0 mg/L DEHP; mix group was exposed to 1.0 μg/L EE2 and 1.0 mg/L DEHP. The experiment continued for 56 days. Fish survival rate was not different among experimental groups. Fish in DEHP and mix groups had the highest weight gain, and lowest value appeared in control group. The highest hepatosomatic index was found in DEHP and mix groups. Serum alanine transaminase of fish in control group was lower than other groups, but the alkaline phosphatase value was the highest. Serum total anti-oxidation capacity, superoxide dismutase and catalase activities of fish in control group were higher than other groups, but malondialdehyde content is opposite. Respiratory burst and phagocytic indices of fish in EE2 group were the lowest. After 96 h of ammonia stress, the survival rate of fish in mix group was significantly lower than control group. This study indicates that EE2 and DEHP exposure can lead to gain weight of yellow catfish, which is related to liver damage and fat accumulation; EE2 and DEHP exerts its toxic effects by inducing ROS generation, leading to lipid peroxidation and immunosuppression.

Effects of acute ammonia toxicity on oxidative stress, immune response and apoptosis of juvenile yellow catfish Pelteobagrus fulvidraco and the mitigation of exogenous taurine

Ammonia can easily form in intensive culture systems due to ammonification of uneaten food and animal excretion, which usually brings detrimental health effects to fish. However, little information is available on the mechanisms of the detrimental effects of ammonia stress and mitigate means in fish. In this study, the four experimental groups were carried out to test the response of yellow catfish to ammonia toxicity and their mitigation through taurine: group 1 was injected with NaCl, group 2 was injected with ammonium acetate, group 3 was injected with ammonium acetate and taurine, and group 4 was injected taurine. The results showed that ammonia poisoning could induce ammonia, glutamine, glutamate and malondialdehyde accumulation, and subsequently lead to blood deterioration (red blood cell, hemoglobin and serum biochemical index reduced), oxidative stress (superoxide dismutase and catalase activities declined) and immunosuppression (lysozyme, 50% hemolytic complement, total immunoglobulin, phagocytic index and respiratory burst reduced), but the exogenous taurine could mitigate the adverse effect of ammonia poisoning. In addition, ammonia poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, CAT, GPx and GR), inflammatory cytokines (TNF, IL-1 and IL-8) and apoptosis (p53, Bax, caspase 3 and caspase 9) genes transcription, suggesting that cell apoptotic and inflammation may relate to oxidative stress. This result will be helpful to understand the mechanism of aquatic toxicology induced by ammonia in fish.

Growth, blood health, antioxidant status, immune response and resistance to Aeromonas hydrophila of juvenile yellow catfish exposed to di-2-ethylhexyl phthalate (DEHP)

Triplicate groups of juvenile yellow catfish Pelteobagrus fulvidraco were exposed to three levels of DEHP (0, 0.1 and 0.5mgL−1) for 56days. Fish survival (100%) was not affected by different levels of ambient DEHP. Final body weight, weight gain, specific growth rate and feed intake of fish exposed to 0.5mgL−1 DEHP were the highest. On the contrary, hepatosomatic index of fish exposed to 0.1 and 0.5mgL−1 DEHP were the lowest. Serum total protein, glutamic-pyruvic transaminase, glutamic-oxaloacetic transaminase, glucose and triglycerides increased with the increasing concentrations of DEHP exposure. Superoxide dismutase and glutathione peroxidase activities of fish exposed to 0.5mgL−1 DEHP were the lowest, but malondialdehyde contents of fish exposed to 0.1 and 0.5mgL−1 DEHP were higher than that of control fish. Phagocytic indices of the control group were the highest. After being intraperitoneally injected with Aeromonas hydrophila, fish in the control group had the highest expression of toll like receptor 5, and the expression of myeloid differentiation factor 88 of fish exposed to 0.5mgL−1 DEHP was the lowest. This study indicates that DEHP exerts its toxic effects by interfering with hepatic metabolism, inducing ROS generation and malondialdehyde accumulation, leading to blood deterioration and immunosuppression.

Growth, blood health, antioxidant status and immune response in juvenile yellow catfish Pelteobagrus fulvidraco exposed to α-ethinylestradiol (EE2)

Triplicate groups of juvenile yellow catfish Pelteobagrus fulvidraco were exposed to three levels of α-ethinylestradiol (EE2) (0, 0.1 and 1 ng L−1) for 56 days. Fish survival rate (>93.33%) was not different among experimental groups. Weight gain and specific growth rate of fish exposed to EE2 were higher than those of control fish. Hepatosomatic index of fish exposed to 1 ng L−1 EE2 was the highest. Serum total protein, albumin, globulin, alanine aminotransferase, aspartate transaminase, cholesterol and triglyceride increased with increasing EE2 exposure levels. Liver total anti-oxidative capacity, malondialdehyde content and lysozyme activity of fish exposed to EE2 were higher than those of control fish. Phagocytic indices of fish exposed to 1 ng L−1 EE2 was lower than that of control fish. This study indicates that although EE2 exposure can promote the growth of yellow catfish in short-term, EE2 exerts its toxic effects by inducing reactive oxygen species generation and malondialdehyde accumulation, leading to blood deterioration and interfering with immune response.

Effects of ammonia on growth, digestion and antioxidant capacity in juvenile yellow catfish Pelteobagrus fulvidraco (Richardson, 1846)

Summary Effects of ammonia stress on food ingestion, growth, digestion and antioxidant capacity were investigated in juvenile yellow catfish Pelteobagrus fulvidraco (Richardson) with initial body weights of 20.24 ± 0.18 g. The fish were reared in triplicate in 15 experimental tanks at a rate of 30 fish per tank for 56 days. Water was maintained at a dissolved oxygen (DO) level of over 6.2 mg L−1, pH 7.2–7.6, and temperature of 29.0 ± 1.5°C under a natural 12L: 12D photoperiod. Survival, food ingestion (FI), specific growth rate (SGR), food conversion efficiency (FCE), apparent digestibility coefficient (ADC), total antioxidant capacity (T-AOC), levels of glutathione (GSH) and malonaldehyde (MDA), and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) of the juveniles were determined in total ammonia nitrogen (NH3-N+NH4-N) levels of 0 (control group), 3.36, 6.72, 13.44 and 26.88 mg L−1. The results show that the survival, FI, SGR, FCE, and ADC decreased significantly with an increase in total ammonia nitrogen (p < .05), and a significantly negative correlation between SGR and total ammonia nitrogen levels (p < .05). T-AOC, SOD, CAT, GSH-PX and GSH in the blood, liver and gills were found to decline significantly with an increase in the total ammonia nitrogen level (p < .05), while the MDA in the blood, liver and gills was elevated significantly with the increase in total ammonia nitrogen (p < .05). The results indicate a threshold in the induction of the T-AOC and activities of antioxidant enzymes in yellow catfish tissues with a total ammonia nitrogen increase. In the present study the total ammonia nitrogen threshold thus changed from 6.72 mg L−1 in the juvenile yellow catfish.

Effect of dietary choline levels on growth performance, lipid deposition and metabolism in juvenile yellow catfish Pelteobagrus fulvidraco.

The present experiment was conducted to determine the effect and mechanism of dietary choline levels on growth performance and lipid deposition of yellow catfish Pelteobagrus fulvidraco. Dietary choline was included at three levels of 239.2 (control (without extra choline addition), 1156.4 and 2273.6mg choline per kg diet, respectively) and fed to yellow catfish (mean initial weight: 3.45±0.02g mean±standard errors of mean (SEM)) for 8weeks. Fish fed the diet containing 1156.4mgkg-1 choline showed the higher weight gain (WG), specific growth rate (SGR) and feed intake (FI), but the lower feed conversion rate (FCR), than those in control and highest choline group. Hepatosomatic index (HSI) and hepatic lipid content declined with increasing dietary choline levels. Muscle lipid content was the lowest for fish fed adequate choline diets and showed no significant difference between other two groups. Choline contents in liver and muscle increased with increasing dietary choline levels. Dietary choline levels significantly influenced mRNA levels of genes involved in lipid homeostasis in muscle and liver, such as CTP:phosphocholine cytidylyltransferase a (CCTa), phosphatidylethanolamine N-methyl-transferase (PEMT), microsomal triglyceride transfer protein (MTP), apolipoprotein b (APOBb), apolipoprotein E (ApoE) and lipoprotein lipase (LPL), and effects of dietary choline levels on lipid deposition and metabolism were tissue-specific. Different responses of these genes at the mRNA levels partially explained the profiles of lipid deposition in liver and muscle for fish fed different choline diets. To our knowledge, this is the first to explore the effect of dietary choline level on mRNA expression of these genes, which provides new insights into choline nutrition in fish.

Ammonia toxicity induces glutamine accumulation, oxidative stress and immunosuppression in juvenile yellow catfish Pelteobagrus fulvidraco

A study was carried to test the response of yellow catfish for 28days under two ammonia concentrations. Weight gain of fish exposure to high and low ammonia abruptly increased at day 3. There were no significant changes in fish physiological indexes and immune responses at different times during 28-day exposure to low ammonia. Fish physiological indexes and immune responses in the treatment of high ammonia were lower than those of fish in the treatment of low ammonia. When fish were exposed to high ammonia, the ammonia concentration in the brain increased by 19-fold on day 1. By comparison, liver ammonia concentration reached its highest level much earlier at hour 12. In spite of a significant increase in brain and liver glutamine concentration, there was no significant change in glutamate level throughout the 28-day period. The total superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione reductase (GR) activities in the brain gradually decreased from hour 0 to day 28. Liver SOD, GPX and GR activities reached the highest levels at hour 12, and then gradually decreased. Thiobarbituric acid reactive substance brain and liver content gradually increased throughout the 28-day period. Lysozyme, acid phosphatase and alkaline phosphatase activities in the liver reached exceptionally low levels after day 14. This study indicated that glutamine accumulation in the brain was not the major cause of ammonia poisoning, the toxic reactive oxygen species is not fully counter acted by the antioxidant enzymes and immunosuppression is a process of gradual accumulation of immunosuppressive factors.

Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco.

We investigated the effects of deficient and excess dietary selenium (Se) on growth, blood cells apoptosis and liver heat shock protein 70 (HSP70) expression in juvenile yellow catfish (Pelteobagrus fulvidraco). After 8 weeks, yellow catfish (initial weight: 2.12 ± 0.01 g) fed isonitrogenous and isolipid diets containing <0.05 (deficient dietary Se) or 6.5 (excess dietary Se) mg Se/kg displayed a significantly lower weight gain ratio (WGR) than those fed a diet containing 0.23 (normal dietary Se) mg Se/kg. As dietary Se levels increased, liver Se concentration, glutathione peroxidase activity and the hepatosomatic index increased significantly. Plasma glucose concentration was highest in the normal treatment compared with the excess dietary Se treatment. Both deficient and excess dietary Se lead to increased reactive oxygen species (ROS) production and apoptosis ratio in blood cells, whereas only excess dietary Se increased their cytoplasmic free-Ca(2+) (CF-Ca(2+)) concentration. Excess dietary Se also resulted in the highest level of HSP70 expression, thereby possibly providing a protective mechanism against oxidative stress. These results indicate that both deficient and excess dietary Se restrained the growth of juvenile yellow catfish and caused oxidative stress. The overproduction of ROS may act as a signal molecule mediate apoptosis when dietary Se deficiency. Both ROS and CF-Ca(2+) were recorded when dietary Se excess, suggesting that Ca(2+) may be activated by Se and play a major role during Se-induced oxidative stress and cell apoptosis.

Effects of dietary taurine on growth, immunity and hyperammonemia in juvenile yellow catfish Pelteobagrus fulvidraco fed all-plant protein diets

An 84-day feeding trial was conducted to determine the dietary taurine requirement of juvenile yellow catfish Pelteobagrus fulvidraco. Six isonitrogenous and isolipidic diets (40% protein and 7% lipid) were formulated to contain six graded dietary taurine levels ranging from 0.02 to 2.55% (dry weight) in about 0.5% increments. Each diet was randomly assigned to triplicate groups of 30 juvenile fish (5.18±0.14g) twice daily to apparent satiation. The results indicated that weight gain and red blood cell, hemoglobin and hematocrit significantly increased as dietary taurine levels increased up to 1.09%, but were not significantly different from 1.09 to 2.55% taurine diets. Serum total protein, triglyceride, cholesterol and alanine aminotransferase decreased with increasing dietary taurine levels, on the contrary, serum superoxide dismutase, catalase and glutathione peroxidase activities, lysozyme activity, phagocytic index, respiratory burst and total immunoglobulin content increased. Fish fed the taurine deficient diet (0.02% of dry diet) showed the highest hepatosomatic index, whole body lipid, white blood cell count and malondialdehyde content. Cumulative mortality in fish fed 0.02–0.48% taurine diets were higher than in fish fed 1.09–2.55% taurine diets after injection with ammonium acetate at hour 24. After the challenge test, fish brain ammonia, glutamate and glutamine contents decreased as dietary taurine levels increased up to 1.09%, but no significant differences were found with a further increase in dietary taurine. The two-straight broken-line regression analysis on weight gain against dietary taurine levels indicated that the optimal dietary taurine requirement was estimated to be 1.09% of the diet. Based on fish growth, immunity and resistance against hyperammonemia, the level of 1.09% taurine in the all-plant protein diet is recommended in juvenile yellow catfish. Statement of relevanceThis study will be useful in developing amino acid-balanced diets for intensive culture of yellow catfish.