South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of South China Sea Fishery Resources Exploitation and Utilization, Ministry of Agriculture and Rural Affairs, Guangzhou 510300, Guangdong Province, China; College of Fisheries, Tianjin Agricultural University, 300384 Tianjin, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), 511458, Guangdong Province, China.
South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of South China Sea Fishery Resources Exploitation and Utilization, Ministry of Agriculture and Rural Affairs, Guangzhou 510300, Guangdong Province, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), 511458, Guangdong Province, China.
Aquat Toxicol. 2021 Nov;240:105969. doi: 10.1016/j.aquatox.2021.105969. Epub 2021 Sep 24.
Continuous exposure to high levels of ammonia can cause oxidative damage to fish tissues and organs. To date, the mechanism by which juvenile golden pompano (Trachinotus ovatus) are poisoned by ammonia exposure has not been thoroughly elucidated. although the mechanisms of ammonia toxicity are not well described for the pompano, many other studies presented these effects to other fish species. So an overview would be given. First, an acute ammonia nitrogen toxicity experiment on juvenile golden pompano obtained a 96-h half-lethal concentration (96 h LC50) of 26.9 mg/L. In the ammonia exposure experiment, fish were sampled at 0 h, 6 h, 12 h, 24 h, 48 h, 72 h and 96 h after exposure to ammonia water (26.93 mg/L). The results showed that with the prolonged ammonia nitrogen exposure, plasma cortisol (COR), total cholesterol (TC), glutamic-pyruvic transaminase (ALT), glutamic oxalacetic transaminase (AST) and malonaldehyde (MDA) levels continued to rise, while glucose (GLU) levels first increased and later gradually decreased after 12 h. The activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in the liver and the mRNA expression levels of antioxidant genes (SOD, CAT, and GPX) first increased and subsequently decreased with increasing exposure time. Through microscopic observation, it was found that the degree of liver damage increased with increasing stress time and was most serious at 96 h. In the post-poison recovery experiment, the fish exposed to ammonia were transferred to clean water, and samples were taken at 24 h, 48 h, 72 h and 96 h after recovery. The results showed that with the increasing recovery time, each index recovered to the initial level to varying degrees, but the recovery time of 96 h was not enough for the fish to return to the normal level. We also examined the regulation of the Nrf2-Keap1 signaling pathway by the molecular mechanism of the antioxidant defense system. The results of this analysis showed that there was a positive correlation between Nrf2 and liver antioxidant gene expression levels, while there was a negative correlation between Keap1 and liver antioxidant gene expression levels, which may be observed because Nrf2 plays a key role in inducing antioxidant genes, and Keap1 may hinder the response to Nrf2. These results may provide a deeper and more comprehensive understanding of the impact of ammonia exposure on fish and help to provide a foundation for managing the healthy reproduction of juvenile fish.
持续暴露在高水平的氨中会对鱼类组织和器官造成氧化损伤。迄今为止，幼年金 pompano（Trachinotus ovatus）被氨暴露毒害的机制尚未得到彻底阐明。尽管氨毒性的机制尚未很好地描述 pompano，但许多其他研究也呈现了这些效应在其他鱼类中的作用。因此，将对此进行概述。首先，对幼年金 pompano 进行了急性氨氮毒性实验，获得了 96 小时半致死浓度（96 h LC50）为 26.9 mg/L。在氨暴露实验中，在暴露于氨（26.93 mg/L）后 0 h、6 h、12 h、24 h、48 h、72 h 和 96 h 时取样。结果表明，随着氨氮暴露时间的延长，血浆皮质醇（COR）、总胆固醇（TC）、谷草转氨酶（ALT）、谷丙转氨酶（AST）和丙二醛（MDA）水平持续升高，而葡萄糖（GLU）水平在 12 h 后先升高后逐渐降低。肝脏中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPX）的活性以及抗氧化基因（SOD、CAT 和 GPX）的 mRNA 表达水平随着暴露时间的增加先升高后降低。通过显微镜观察发现，肝损伤程度随应激时间的增加而增加，96 h 时最为严重。在中毒后恢复实验中，将暴露于氨的鱼转移到清洁水中，在恢复后 24 h、48 h、72 h 和 96 h 取样。结果表明，随着恢复时间的增加，各指标在不同程度上恢复到初始水平，但 96 h 的恢复时间不足以使鱼恢复到正常水平。我们还研究了 Nrf2-Keap1 信号通路对抗氧化防御系统分子机制的调节。分析结果表明，Nrf2 与肝脏抗氧化基因表达水平呈正相关，而 Keap1 与肝脏抗氧化基因表达水平呈负相关，这可能是因为 Nrf2 对诱导抗氧化基因起关键作用，而 Keap1 可能会阻碍对 Nrf2 的反应。这些结果可能为深入了解氨暴露对鱼类的影响提供更全面的认识，并有助于为管理幼鱼的健康繁殖提供基础。
