Abstract：
Exposure to ammonia can cause convulsions, coma, and death. In this study, we investigate the effects of ammonia exposure on immunoregulatory and neuroendocrine changes in Takifugu rubripes. Fish were sampled at 0, 12, 24, 48, and 96 h following exposure to different ammonia concentrations (0, 5, 50, 100, and 150 mg/L). Our results showed that exposure to ammonia significantly reduced the concentrations of C3, C4, IgM, and LZM whereas the heat shock protein 70 and 90 levels significantly increased. In addition, the transcription levels of Mn-SOD, CAT, GRx, and GR in the liver were significantly upregulated following exposure to low ammonia concertation, however, downregulated with increased exposure time. These findings suggest that ammonia poisoning causes oxidative damage and suppresses plasma immunity. Ammonia exposure also resulted in the elevation and depletion of the T3 and T4 levels, respectively. Furthermore, ammonia stress induced an increase in the corticotrophin-releasing hormone, adrenocorticotropic hormone, and cortisol levels, and a decrease in dopamine, noradrenaline, and 5-hydroxytryptamine levels in the brain, illustrating that ammonia poisoning can disrupt the endocrine and neurotransmitter systems. Our results provide insights into the mechanisms underlying the neurotoxic effects of ammonia exposure, which helps to assess the ecological and environmental health risks of this contaminant in marine fish.
摘要：
接触氨会引起抽搐,昏迷,和死亡。在这项研究中,我们研究了氨暴露对Takifugurubbrips免疫调节和神经内分泌变化的影响。在暴露于不同氨浓度（0、5、50、100和150mg/L）后的0、12、24、48和96小时对鱼类进行采样。我们的结果表明，暴露于氨显著降低C3，C4，IgM的浓度，和LZM，而热休克蛋白70和90水平显着增加。此外,Mn-SOD的转录水平，CAT,GRx,肝脏中的GR在暴露于低氨浓度后显著上调，然而,随着暴露时间的增加而下调。这些发现表明氨中毒会引起氧化损伤并抑制血浆免疫力。氨暴露也导致T3和T4水平的升高和耗尽，分别。此外，氨胁迫诱导促肾上腺皮质激素释放激素的增加，促肾上腺皮质激素,和皮质醇水平，多巴胺的减少，去甲肾上腺素,和大脑中的5-羟色胺水平，说明氨中毒会破坏内分泌和神经递质系统。我们的结果提供了对氨暴露的神经毒性作用的潜在机制的见解，这有助于评估海洋鱼类中这种污染物的生态和环境健康风险。
