Jiangsu Key Laboratory of Marine Biotechnology/Laboratory of Pathology and Immunology of Aquatic Animals, Jiangsu Ocean University, Lianyungang 222005, China; Co-Innovation Center of Jiangsu Marine Bio-Industry Technology, Lianyungang 222005, China.
Jiangsu Key Laboratory of Marine Biotechnology/Laboratory of Pathology and Immunology of Aquatic Animals, Jiangsu Ocean University, Lianyungang 222005, China.
Aquat Toxicol. 2022 Oct;251:106280. doi: 10.1016/j.aquatox.2022.106280. Epub 2022 Aug 24.
Nitrate (NO) pollution of waterbodies has attracted significant global attention as it poses a serious threat to aquatic organisms and human beings. This study aimed to evaluate the role of NO, an end product of biological nitrification processes, in immune status and lipid metabolism to have a comprehensive understanding of its toxic effects on fishes. Therefore, in this work, juvenile turbot (Scophthalmus maximus) were subjected to four nominal concentrations of NO (i.e., 0, 50, 200, 400 mg/L of NO-N) for a 60-day period. The results indicated that increased exposure to NO (200 and/or 400 mg/L) enhanced the concentrations of plasma heat shock protein concentrations (HSP70), complement component 3 (C3), complement component 4 (C4), immunoglobulin M (IgM) and lysozyme (LYS), which meant that NOcaused fluctuations in the plasma immune system. Higher exposure to NO (200 and/or 400 mg/L) also caused significant enhancements in plasma glutamic pyruvic transaminase (GPT), as well as glutamic oxaloacetic transaminase (GOT) activity. Furthermore, NO exposure resulted in upregulation of liver TNF-α, IL-1β, HSP70, HSP90, and LYS. Additionally, the results suggested that NOexposure caused a certain degree of histological damage and inflammation in the liver and activated the immune defense processes of juvenile turbot. Furthermore, the mRNA expression levels of certain genes associated with lipid metabolism (peroxisome proliferator-activated receptor-alpha [PPAR-α], carnitine palmitoyltransferase 1[CPT1], liver X receptor [LXR] together with sterol regulatory element binding protein-1 [SREBP-1]) increased significantly within fish liver exposed to 200/400 mg/L NO-N treatments. Finally, the results obtained from the analysis of the integrated biological responses version 2 (IBRv2) also confirmed the toxic effects of NO on juvenile turbot. According to these findings, it can be found that NO emission in the aquatic environment needs to be strictly controlled, as it may cause immune and lipid metabolism disorders in fish.
水体中硝酸盐（NO）的污染已引起全球高度关注，因为它对水生生物和人类构成了严重威胁。本研究旨在评估作为生物硝化过程的终产物的 NO 在免疫状态和脂质代谢中的作用，以便全面了解其对鱼类的毒性影响。因此，在这项工作中，将大菱鲆（Scophthalmus maximus）幼鱼暴露于四个名义浓度的 NO（即 0、50、200、400mg/L 的 NO-N）下 60 天。结果表明，增加 NO（200 和/或 400mg/L）暴露会增加血浆热休克蛋白浓度（HSP70）、补体成分 3（C3）、补体成分 4（C4）、免疫球蛋白 M（IgM）和溶菌酶（LYS）的浓度，这意味着 NO 引起了血浆免疫系统的波动。更高的 NO（200 和/或 400mg/L）暴露还会导致血浆谷氨酸丙酮酸转氨酶（GPT）和谷氨酸草酰乙酸转氨酶（GOT）活性显著增强。此外，NO 暴露会导致肝脏 TNF-α、IL-1β、HSP70、HSP90 和 LYS 的表达上调。此外，结果表明，NO 暴露会对大菱鲆肝脏造成一定程度的组织损伤和炎症，并激活其免疫防御过程。此外，与脂质代谢相关的某些基因（过氧化物酶体增殖物激活受体-α[PPAR-α]、肉碱棕榈酰转移酶 1[CPT1]、肝 X 受体[LXR]与固醇调节元件结合蛋白-1[SREBP-1]）的 mRNA 表达水平在暴露于 200/400mg/L NO-N 处理的鱼肝脏中显著增加。最后，综合生物反应版本 2（IBRv2）分析得到的结果也证实了 NO 对大菱鲆的毒性影响。根据这些发现，可以发现需要严格控制水环境污染中的 NO 排放，因为它可能会导致鱼类的免疫和脂质代谢紊乱。
