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 (NH4+-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.

中文翻译：

---

氨暴露和太平洋白虾 Litopenaeus vannamei 暴露后恢复的影响：组织学、生理学和分子反应


氨暴露对南美白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，但南滨对虾从氨损伤中恢复的能力仍不清楚。为了进一步了解南美白乳杆菌对氨的适应机制，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 （NH4+-N 25 mg/L） 和回收实验中，对虾分别在暴露 0 h、24 h、48 h 和回收 24 h、48 h 取样。结果显示，短期氨暴露对肝胰腺和鳃的组织病理学损伤可在恢复后减轻。氨暴露抑制了虾的超氧化物歧化酶 （SOD） 和过氧化氢酶 （CAT） 活性，降低了总抗氧化能力 （T-AOC），增加了丙二醛 （MDA）。暴露后抗氧化系统的恢复减轻了氧化损伤并降低了 MDA 水平。氨暴露对虾酸性磷酸酶 （ACP） 和碱性磷酸酶 （AKP） 活性的抑制是可逆的。氨的排泄和代谢减轻了凡纳滨对虾的氨毒性并促进了恢复。转录组分析在应激 48 h、 24 h 和 48 h 恢复时肝胰腺中分别鉴定了 1690 、 1568 和 1463 个差异表达基因 （DEGs）。KEGG 富集分析显示，氨暴露诱导氧化损伤，导致细胞凋亡。此外，抗氧化剂相关途径的激活，如谷胱甘肽代谢和过氧化物酶体，有助于减少暴露后恢复期的氧化损伤。 添加外源性精胺和亚精胺可能有助于凡纳滨对虾暴露后恢复并增强氨驯化。通过转录组分析筛选的炎症基因 STEAP4 在氨应激和恢复期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的可逆性，补充了虾在氨暴露下的适应机制知识，并为后续甲壳类动物的氨耐受性研究提供了基础。