College of Fisheries, Guangdong Ocean University, Zhanjiang, 524088, China; Guangdong Provincial Shrimp Breeding and Culture Laboratory, Guangdong Ocean University, Zhanjiang, 524088, China.
College of Fisheries, Guangdong Ocean University, Zhanjiang, 524088, China; Guangdong Provincial Shrimp Breeding and Culture Laboratory, Guangdong Ocean University, Zhanjiang, 524088, China.
Aquat Toxicol. 2024 Dec;277:107133. doi: 10.1016/j.aquatox.2024.107133. Epub 2024 Oct 28.
The toxic effects of ammonia exposure on Litopenaeus vannamei have been widely reported, including tissue damage, oxidative stress, and metabolic disorders, but the ability of L. vannamei to recover from ammonia damage is still unclear. To further understand the adaptation mechanism of L. vannamei to ammonia, this study explored the effects of ammonia exposure and recovery on histopathology, physiological indicators, and transcriptomic responses. In the ammonia exposure (NH-N 25 mg/L) and recovery experiment, shrimp were sampled at 0 h, 24 h, 48 h of exposure, and 24 h, 48 h of recovery. The results showed that histopathological damage to the hepatopancreas and gills caused by short-term ammonia exposure could be alleviated after recovery. Ammonia exposure inhibited superoxide dismutase (SOD) and catalase (CAT) activities, decreased total antioxidant capacity (T-AOC), and increased malondialdehyde (MDA) in shrimp. Restoration of the antioxidant system after exposure mitigated oxidative damage and reduced MDA levels. The inhibition of acid phosphatase (ACP) and alkaline phosphatase (AKP) activities in shrimp caused by ammonia exposure was reversible. Ammonia excretion and metabolism attenuate ammonia toxicity and promote recovery in L. vannamei. Transcriptome analysis identified 1690, 1568, and 1463 differentially expressed genes (DEGs) in the hepatopancreas at 48 h of stress, 24 h, and 48 h of recovery, respectively. KEGG enrichment analysis revealed that ammonia exposure induced oxidative damage, resulting in apoptosis. Furthermore, activation of antioxidant-related pathways, such as glutathione metabolism and peroxisomes, helped reduce oxidative damage during the post-exposure recovery period. The addition of exogenous spermine and spermidine may contribute to post-exposure recovery and enhance ammonia acclimation in L. vannamei. Differential expression of the inflammatory gene STEAP4 in the ammonia stress and recovery phases, as screened by transcriptome analysis, may play a positive role in post-stress recovery. This study demonstrated the reversibility of the toxic effects of ammonia exposure on L. vannamei, complemented the knowledge of the mechanisms of adaptation of shrimp under ammonia exposure, and provided a basis for subsequent ammonia tolerance studies in crustaceans.
氨暴露对凡纳滨对虾的毒性作用已被广泛报道，包括组织损伤、氧化应激和代谢紊乱，但对凡纳滨对虾从氨损伤中恢复的能力仍不清楚。为了进一步了解凡纳滨对虾适应氨的机制，本研究探讨了氨暴露和恢复对组织病理学、生理指标和转录组反应的影响。在氨暴露（NH-N 25mg/L）和恢复实验中，分别在暴露 0h、24h、48h 和恢复 24h、48h 时采样虾。结果表明，短期氨暴露引起的肝胰腺和鳃组织病理学损伤在恢复后可得到缓解。氨暴露抑制了虾超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，降低了总抗氧化能力（T-AOC），增加了丙二醛（MDA）的含量。暴露后抗氧化系统的恢复减轻了氧化损伤，降低了 MDA 水平。氨暴露抑制虾酸性磷酸酶（ACP）和碱性磷酸酶（AKP）的活性是可逆的。氨排泄和代谢减轻了凡纳滨对虾的氨毒性，促进了其恢复。转录组分析鉴定了肝胰腺在应激 48h、恢复 24h 和 48h 时分别有 1690、1568 和 1463 个差异表达基因（DEGs）。KEGG 富集分析表明，氨暴露诱导氧化损伤，导致细胞凋亡。此外，抗氧化相关途径如谷胱甘肽代谢和过氧化物酶体的激活有助于减少暴露后恢复期间的氧化损伤。外源性腐胺和亚精胺的添加可能有助于暴露后的恢复，并增强凡纳滨对虾的氨适应能力。转录组分析筛选出的炎症基因 STEAP4 在氨胁迫和恢复阶段的差异表达可能在应激后恢复中发挥积极作用。本研究证明了氨暴露对凡纳滨对虾的毒性作用具有可逆性，补充了虾在氨暴露下适应机制的知识，为甲壳类动物后续的氨耐受研究提供了依据。
