Abstract：
Nitrite is one of the most common toxic pollutants in intensive aquaculture and is harmful to aquatic animals. Recovery mechanisms post exposure to nitrite in shrimp have rarely been investigated. This study focuses on the effect of nitrite exposure and post-exposure recovery on the histological and physiological aspects of Litopenaeus vannamei and utilizes transcriptome sequencing to analyze the molecular mechanisms of adaptation to nitrite exposure. The results showed that histopathological damage to the hepatopancreas and gills caused by short-term nitrite exposure resolved with recovery. The total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and catalase (CAT) of shrimp were significantly reduced during nitrite exposure and returned to the control level after recovery, malondialdehyde (MDA) levels were opposite to them. Restoration of the antioxidant system after exposure mitigated oxidative damage. Nitrite exposure results in reduced activity of the immuno-enzymes acid phosphatase (ACP) and alkaline phosphatase (AKP), which can be recovered to the control level. L. vannamei can adapt to nitrite exposure by regulating Na+/K+-ATPase (NKA) activity. Transcriptome analysis revealed that activation of glutathione metabolism and peroxisomal pathways facilitated the mitigation of oxidative damage in L. vannamei during the recovery period. Excessive oxidative damage activates the apoptosis and p53 pathways. Additionally, Sestrin2 and STEAP4 may have a positive effect on recovery in shrimp. These results provide evidence for the damage caused by nitrite exposure and the recovery ability of L. vannamei. This study can complement the knowledge of the mechanisms of adaptation and recovery of shrimp under nitrite exposure.
摘要：
亚硝酸盐是集约化水产养殖中最常见的有毒污染物之一，对水生动物有害。很少研究虾暴露于亚硝酸盐后的恢复机制。本研究重点研究亚硝酸盐暴露和暴露后恢复对凡纳滨对虾组织学和生理方面的影响，并利用转录组测序分析适应亚硝酸盐暴露的分子机制。结果表明，短期亚硝酸盐暴露对肝胰腺和g的组织病理学损害随着恢复而解决。总抗氧化能力（T-AOC），超氧化物歧化酶（SOD），和过氧化氢酶（CAT）的虾在亚硝酸盐暴露期间显着降低，恢复后恢复到对照水平，丙二醛（MDA）水平与它们相反。暴露后抗氧化系统的恢复减轻了氧化损伤。亚硝酸盐暴露导致免疫酶酸性磷酸酶（ACP）和碱性磷酸酶（AKP）的活性降低，可以恢复到控制水平。南美白对虾可以通过调节Na+/K+-ATP酶(NKA)活性来适应亚硝酸盐暴露。转录组分析显示，谷胱甘肽代谢和过氧化物酶体途径的激活有助于在恢复期缓解凡纳滨对虾的氧化损伤。过度氧化损伤激活细胞凋亡和p53途径。此外,Sestrin2和STEAP4可能对虾的恢复具有积极作用。这些结果为亚硝酸盐暴露造成的伤害和南美白对虾的恢复能力提供了证据。这项研究可以补充对虾在亚硝酸盐暴露下的适应和恢复机制的知识。
