Ammonia is toxic to most fish, and its negative effects can be eliminated by nutritional manipulation. In this study, triplicate groups of yellow catfish (0.58 ± 0.03 g) were fed diets supplemented with 0, 0.30 and 0.60 mg selenium (Se) kg⁻¹ diet for 56 days under three ammonia contents (0.00, 5.70 and 11.40 mg L⁻¹ total ammonia nitrogen). The results showed that ammonia toxicity could affects growth (weight gain, feed efficiency ratio, Se contents in muscle and whole body declined) and survival, leads to oxidative stress (total antioxidant capacity, superoxide dismutase, catalase and glutathione peroxidase activities declined and malondialdehyde accumulation), immunosuppression (lysozyme activity, 50% hemolytic complement, immunoglobulin M, respiratory burst and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 elevated), induces up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNFα, IL 1 and IL 8) and pro-apoptotic genes (p53, Bax, Cytochrome c, Caspase 3 and Caspase 9) transcription, and down-regulation of anti-apoptotic gene Bcl2 transcription. The dietary Se supplementation could mitigate the adverse effect of ammonia poisoning on fish growth, oxidative damage, immunosuppression and apoptotic.

氨对大多数鱼类有毒，可以通过营养处理消除其负面影响。在这项研究中，一式三份的黄色cat鱼（0.58±0.03 g）在三种氨含量（0.00、5.70和11.40 mg L-的条件下）饲喂了补充有0、0.30和0.60 mg硒（Se）kg ^-1饮食的56天^{。 1个}总氨氮）。结果表明，氨中毒会影响生长（体重增加，饲料效率比，肌肉和全身中的硒含量降低）和存活率，并导致氧化应激（总抗氧化能力，超氧化物歧化酶，过氧化氢酶和谷胱甘肽过氧化物酶活性下降和丙二醛积累） ），免疫抑制（溶菌酶活性，50％溶血补体，免疫球蛋白M，呼吸爆发和吞噬指数降低）和细胞因子释放（TNF，IL 1和IL 8升高）诱导抗氧化酶的上调（Cu / Zn-SOD，Mn-SOD，CAT和GPx），细胞因子（TNFα，IL 1和IL 8）和促凋亡基因（p53，Bax，细胞色素c，Caspase 3和Caspase 9）的转录，以及抗凋亡基因Bcl2转录的下调。膳食中硒的补充可以减轻氨中毒对鱼类生长，氧化损伤，免疫抑制和细胞凋亡的不利影响。