Aquaculture Reports ( IF 3.7 ) Pub Date : 2021-05-18 , DOI: 10.1016/j.aqrep.2021.100722 Shenping Cao , Dafang Zhao , Rong Huang , Yangbo Xiao , Wenqian Xu , Xunxin Liu , Yang Gui , Shitao Li , Jiahui Xu , Jianzhou Tang , Fufa Qu , Zhen Liu , Shaojun Liu
This study was conducted to evaluate the effect of acute ammonia stress on intestinal oxidative stress levels, histology, and activity of digestive enzymes and oligopeptide transporter 1 (PepT1) in grass carp. Three concentrations of ammonia nitrogen: 0 mg/L total ammonia nitrogen (TAN) (the control group), 1.7 mg/L TAN were used in the present study. Fish were sampled at 0 h, 12 h, 24 h, and 48 h after exposure to ammonia. The results showed that the activities of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT) and the content of cortisol were all increased in fish exposed to the two concentrations of TAN. Compared with the control group, the activities of intestinal trypsin and chymotrypsin significantly increased in the 1.7 mg/L TAN group, while amylase activity was significantly suppressed in the 50 mg/L TAN group. After ammonia exposure, the expression of intestinal Nrf2 gene significantly increased in the 1.7 mg/L TAN group while the expression of Keap1 gene significantly increased in the 50 mg/L TAN group. Moreover, the expression of intestinal PepT1, Sp1 and CDX2 significantly increased after fish exposed to 1.7 mg/L TAN. The width of mid-intestine villi of fish from the 50 mg/L TAN group was significantly higher than fish from the other two groups. Meanwhile, the area density of PepT1 in the 50 mg/L TAN group was significantly smaller than that in the control and 1.7 mg/L TAN groups. The results suggested that ammonia stress induces intestinal oxidative stress, and 1.7 mg/L TAN increased the expressions of PepT1-related genes and the activities of the intestinal trypsin and chymotrypsin. This conclusion indicates that ammonia nitrogen stress affects the intestinal digestion and absorption performance of aquatic animals, and reducing ammonia nitrogen to a suitable level can improve the protein digestion ability of animals.
中文翻译:
急性氨应激对肠道的氧化应激,组织学,消化酶活性和草鱼PEPT1活动的影响(草鱼)
本研究旨在评估急性氨胁迫对草鱼肠道氧化应激水平,组织学以及消化酶和寡肽转运蛋白1(PepT1)活性的影响。本研究使用三种浓度的氨氮:总氨氮(TA N)为0 mg / L ,对照组为1.7 mg / L TAN 。暴露于氨水后的0、12、24和48小时对鱼进行采样。结果表明,暴露于两种浓度的TA N中的鱼的活性氧(ROS)活性,超氧化物歧化酶(SOD),过氧化氢酶(CAT)和皮质醇含量均增加。1.7 mg / L TA中肠胰蛋白酶和胰凝乳蛋白酶的活性显着增加N组,而淀粉酶活性在50 mg / L TA N组中被显着抑制。氨暴露后,肠道Nrf2基因的表达在1.7 mg / L TA N组显着增加,而Keap1基因的表达在50 mg / L TA N组中显着增加。此外,鱼暴露于1.7 mg / L TA N后,肠道PepT1,Sp1和CDX2的表达显着增加。50mg / L TA N组鱼的肠中绒毛宽度显着高于其他鱼两组。同时,PepT1在50 mg / L TA中的面积密度N组显着小于对照组和1.7 mg / L TA N组。结果表明,氨胁迫可引起肠道氧化应激,而1.7 mg / L TA N可增加PepT1相关基因的表达以及肠胰蛋白酶和胰凝乳蛋白酶的活性。该结论表明氨氮胁迫影响水生动物的肠道消化吸收性能,将氨氮降低至适当水平可以提高动物的蛋白质消化能力。