Rixin Wang

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 28 days 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.

The protective effects of taurine on acute ammonia toxicity in grass carp Ctenopharynodon idellus

The four experimental groups were carried out to test the response of grass carp Ctenopharyngodon idella to ammonia toxicity and 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. Fish in group 2 had the highest ammonia content in the liver and brain, and alanine, arginine, glutamine, glutamate and glycine contents in liver. Brain alanine and glutamate of fish in group 2 were significantly higher than those of fish in group 1. Malondialdehyde content of fish in group 2 was the highest, but superoxide dismutase and glutathione activities were the lowest. Although fish in group 2 had the lowest red cell count and hemoglobin, the highest alkaline phosphatase, complement C3, C4 and total immunoglobulin contents appeared in this group. In addition, superoxide dismutase and glutathione activities, red cell count and hemoglobin of fish in group 3 were significantly higher than those of fish in group 2, but malondialdehyde content is the opposite. This study indicates that ammonia exerts its toxic effects by interfering with amino acid transport, inducing reactive oxygen species generation and malondialdehyde accumulation, leading to blood deterioration and over-activation of immune response. The exogenous taurine could mitigate the adverse effect of high ammonia level on fish physiological disorder.

Acute ammonia toxicity in crucian carp Carassius auratus and effects of taurine on hyperammonemia.

The four experimental groups were carried out to test the response of crucian carp Carassius auratus to ammonia toxicity and 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 with taurine. Fish in group 2 had the highest ammonia and glutamine contents, and the lowest glutamate content in liver and brain. Serum superoxide dismutase (SOD), glutathione (GSH) activities, red cell count (RBC), white cell count (WBC), lysozyme (LYZ) activity, complement C3 content of fish in group 2 reflected the lowest, but malondialdehyde content was the highest. Importantly, serum SOD and GSH activites, RBC, WBC, and LYZ activity, C3, C4 and total immunoglobulin contents of fish in group 3 were significantly higher than those of fish in group 2. This study indicates that ammonia exerts its toxic effects by interfering with amino acid transport, inducing ROS generation, leading to malondialdehyde accumulation and immunosuppression of crucian carp. The exogenous taurine could mitigate the adverse effect of high ammonia level on fish physiological disorder.

Di‐2‐ethylhexyl phthalate (DEHP) exposure disturbs lipid metabolism in juvenile yellow catfish Tachysurus fulvidraco

This study was conducted to determine the mechanism by which di-2-ethylhexyl phthalate (DEHP) exposure influences lipid metabolism of juvenile yellow catfish Tachysurus fulvidraco. Fish were exposed to three DEHP concentrations (0, 0·1 and 0·5 mg l-1 DEHP) for 8 weeks. Fatty acid synthase (FAS) activity significantly decreased with increasing DEHP concentrations, the highest value was in the Tween control group, whereas the lowest activities of carnitine palmitoyltransferase (CPT) and lipoprotein lipase (LPL) were in this group. The messenger (m)RNA levels of 6-phospho-gluconate dehydrogenase (6PGD), FAS and acetyl-CoA carboxylase a (ACCa) significantly increased with increasing DEHP concentration, the highest values were in the 0·5 mg l-1 DEHP group. The mRNA level of peroxisome proliferator-activated receptor γ (PPARγ) was lower in Tween control than in fish exposed to 0·1 and 0·5 mg l-1 DEHP. The highest mRNA level of ACCb was in the 0·1 mg l-1 DEHP group. These results indicate that DEHP exposure can disturb lipid metabolism at the enzymatic and mRNA levels in Pelteobagrus fulvidraco.

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.

Modulation of lipid metabolism in juvenile yellow catfish (Pelteobagrus fulvidraco) as affected by feeding frequency and environmental ammonia

In the intensive culture systems, excessive feeding leads to ammonia accumulation, which results in lipid metabolism disorder. However, little information is available on the modulation of lipid metabolism in fish as affected by feeding frequency and ammonia stress. In this study, weight gain increased as feeding frequency increased from one to four times daily, but feed conversion ratio is opposite. The highest survival was found in ammonia group when fish was fed two times daily. Liver ammonia content increased as feeding frequency increased from one to four times daily, and the highest brain ammonia content was found when fish was fed four times daily. The highest liver 6-phospho-gluconate dehydrogenase (6PGD), fatty acid synthase (FAS), carnitine palmitoyltransferase (CPT), and lipoprotein lipase (LPL) contents were found in control group when fish was fed four times daily; in comparison, the highest liver 6PGD, FAS, CPT, and LPL contents were found in ammonia group when fish was fed two times daily. Liver 6PGD, FAS, CPT 1, SREBP-1, and PPARα mRNA expression in control group increased significantly as feeding frequency increased from one to four times daily, and the highest expression of 6PGD, G6PD, and FAS was observed in ammonia group when fish was fed two times daily. This study indicated that the optimal feeding frequency is two times daily when yellow catfish exposed to ammonia.

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

ABSTRACT 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. HIGHLIGHTSAmmonia poisoning induces oxidative stress and inflammation.High blood ammonia level leads cell apoptotic.The exogenous taurine could mitigate the adverse effect.

Effect of dietary alanyl-glutamine dipeptide against chronic ammonia stress induced hyperammonemia in the juvenile yellow catfish (Pelteobagrus fulvidraco)

Triplicate groups of juvenile yellow catfish (1.98 ± 0.01 g) were fed diets supplemented with 0% and 1% alanyl-glutamine dipeptide (AGD) for 56 days under three ammonia concentrations (0.01, 5.70 and 11.40 mg L-1 total ammonia nitrogen). The results showed that ammonia poisoning could induce growth (weight gain and specific growth rate) and survival reduction, live ammonia and serum malondialdehyde accumulation, and subsequently lead to blood deterioration (serum total protein, albumin, globulin, alkaline phosphatase and acid phosphatase reduced), oxidative stress (superoxide dismutase and glutathione peroxidase activities declined), and induce down-regulation of antioxidant enzymes (SOD, GPX and GRX) genes transcription. However, dietary supplemented with 1% AGD could mitigate the adverse effect of ammonia poisoning on fish growth performance.