Waterborne ammonia is an environmental pollutant that is toxic to all aquatic animals. However, ammonia induced toxicity as well as compensatory mechanisms to defend against high environmental ammonia (HEA) are not well documented at present for largemouth bass (Micropterus salmoides), a high value fish for culture and sport fisheries in the United States. To provide primary information on the sensitivity of this species to ammonia toxicity, a 96 h-LC₅₀ test was conducted. Thereafter, responses at physiological, ion-regulatory and transcript levels were determined to get insights into the underlying adaptive strategies to ammonia toxicity. For this purpose, fish were progressively exposed to HEA (8.31 mg/L representing 25% of 96 h-LC₅₀) for 3, 7, 14, 21 and 28 days. Temporal effects of HEA on oxygen consumption rate (MO₂), ammonia and urea dynamics, plasma ions (Na⁺, Cl⁻ and K⁺), branchial Na⁺/K⁺-ATPase (NKA) and H⁺-ATPase activity, muscle water content (MWC), energy store (glycogen, lipid and protein) as well as branchial mRNA expression of Rhesus (Rh) glycoproteins were assessed. Probit analysis showed that 96 h-LC₅₀ of (total) ammonia (as NH₄HCO₃) at 25 °C and pH 7.8 was 33.24 mg/L. Results from sub-lethal end-points shows that ammonia excretion rate (J_amm) was strongly inhibited after 7 days of HEA, but was unaffected at 3, 14 and 21 days. At 28 days fish were able to increase J_amm efficiently and concurrently, plasma ammonia re-established to the basal level. Urea production was increased as evidenced by a considerable elevation of plasma urea, but urea excretion rate remained unaltered. Expression of Rhcg isoform (Rhcg2) mRNA was up-regulated in parallel with restored or increased J_amm, suggesting its ammonia excreting role in largemouth bass. Exposure to HEA also displayed pronounced augmentations in NKA activity, exemplified by a rise in plasma [Na⁺]. Furthermore, [K⁺], [Cl⁻] and MWC homeostasis were disrupted followed by recovery to the control levels. H⁺-ATPase activity was elevated but NKA did not appear to function preferentially as a Na⁺/NH₄⁺-ATPase. From 14 days onwards MO₂ was depressed, potentially an attempt towards minimizing catabolism. Glycogen content in liver and muscle were temporarily depleted, whereas a remarkable increment in protein was evident at the last exposure period. Overall, these data suggest that ammonia induced toxicity can disturb several biological processes in largemouth bass, however, it can adapt to the long-term sub-lethal ammonia concentrations by activating various components of ammonia excretory, ion-regulatory and metabolic pathways.

水性氨是对所有水生动物有毒的环境污染物。但是，目前尚无关于氨引起的毒性以及抵御高环境氨（HEA）的补偿机制的证据，这对于大口黑鲈（Micropterus salmoides）是一种用于美国养殖和体育渔业的高价值鱼类。为了提供有关该物种对氨毒性的敏感性的主要信息，进行了96 h-LC ₅₀测试。此后，确定在生理，离子调节和转录水平上的反应，以深入了解潜在的氨毒性适应策略。为此，将鱼逐渐暴露于HEA（8.31 mg / L，代表96 h-LC _50的25％），持续3、7、14、21和28天。HEA对氧消耗速率（MO时间效应₂），氨和尿素动力学，等离子体离子（Na ⁺，氯^-和K ⁺，鳃的Na）⁺ / K ⁺ -ATP酶（NKA）和H ⁺ -ATP酶活性，肌肉评估了水的含量（MWC），能量存储（糖原，脂质和蛋白质）以及恒河猴（Rh）糖蛋白的分支mRNA表达。概率分析表明，在25°C和pH值为7.8的情况下，（总）氨（以NH ₄ HCO _3形式）的96 h-LC ₅₀为33.24 mg / L。亚致死终点的结果表明，氨的排泄率（J _ammHEA 7天后）被强烈抑制，但在3、14和21天未受影响。在第28天，鱼能够有效并同时增加J _amm，血浆氨重新建立到基础水平。血浆尿素的显着升高证明尿素产量增加，但尿素排泄率保持不变。Rhcg亚型（Rhcg2）mRNA的表达与J _amm的恢复或增加平行_上调，表明其氨在大口_黑鲈中排泄。暴露于HEA还显示出NKA活性明显增强，例如血浆[Na ⁺ ]升高。此外，[K ⁺ ]，[氯^-]和MWC体内平衡被破坏，然后恢复到对照水平。H ⁺ -ATPase活性升高，但NKA似乎没有优先作为Na ⁺ / NH ₄ ⁺ -ATPase起作用。从14天开始，MO ₂被抑制，可能是试图将分解代谢降至最低。肝脏和肌肉中的糖原含量暂时耗尽，而蛋白质的显着增加在最后暴露期明显。总体而言，这些数据表明氨引起的毒性可以干扰大嘴鲈的几种生物过程，但是，它可以通过激活氨的排泄，离子调节和代谢途径的各种成分来适应长期的亚致死氨浓度。