Zou Yuning, Chen Weixing, Xia Banghua, Xiang Yifang, Shen Zhentao, Han Ying, Xue Shuqun
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.
Toxics. 2023 Mar 5;11(3):243. doi: 10.3390/toxics11030243.
Ammonia is one of the main environmental pollutants that affect the survival and growth of fish. The toxic effects on blood biochemistry, oxidative stress, immunity, and stress response of bighead carp () under ammonia exposure were studied. Bighead carp were exposed to total ammonia nitrogen (TAN) concentrations of 0 mg/L, 3.955 mg/L, 7.91 mg/L, 11.865 mg/L, and 15.82 mg/L for 96 h. The results showed that ammonia exposure significantly reduced hemoglobin, hematocrit, red blood cell, white blood cell count, and platelet count and significantly increased the plasma calcium level of carp. Serum total protein, albumin, glucose, aspartate aminotransferase, and alanine aminotransferase changed significantly after ammonia exposure. Ammonia exposure can induce intracellular reactive oxygen species (ROS), and the gene expression of antioxidant enzymes (Mn-SOD, CAT, and GPx) increases at the initial stage of ammonia exposure, while MDA accumulates and antioxidant enzyme activity decreases after ammonia stress. Ammonia poisoning changes the gene expression of inflammatory cytokines; promotes the gene expression of inflammatory cytokines TNF-α, IL-6, IL-12, and IL-1β; and inhibits IL-10. Furthermore, ammonia exposure led to increases in stress indexes such as cortisol, blood glucose, adrenaline, and T3, and increases in heat shock protein 70 and heat shock protein 90 content and gene expression. Ammonia exposure caused oxidative stress, immunosuppression, inflammation, and a stress reaction in bighead carp.
氨是影响鱼类生存和生长的主要环境污染物之一。研究了氨暴露对鳙鱼血液生化、氧化应激、免疫和应激反应的毒性作用。将鳙鱼暴露于总氨氮(TAN)浓度为0 mg/L、3.955 mg/L、7.91 mg/L、11.865 mg/L和15.82 mg/L的环境中96小时。结果表明,氨暴露显著降低了鳙鱼的血红蛋白、血细胞比容、红细胞、白细胞计数和血小板计数,并显著提高了血浆钙水平。氨暴露后,血清总蛋白、白蛋白、葡萄糖、天冬氨酸转氨酶和丙氨酸转氨酶发生了显著变化。氨暴露可诱导细胞内活性氧(ROS),抗氧化酶(Mn-SOD、CAT和GPx)的基因表达在氨暴露初期增加,而丙二醛(MDA)积累,氨应激后抗氧化酶活性降低。氨中毒改变了炎性细胞因子的基因表达;促进了炎性细胞因子TNF-α、IL-6、IL-12和IL-1β的基因表达;并抑制了IL-10。此外,氨暴露导致皮质醇、血糖、肾上腺素和T3等应激指标升高,热休克蛋白70和热休克蛋白90含量及基因表达增加。氨暴露对鳙鱼造成了氧化应激、免疫抑制、炎症和应激反应。