RESUMO
Nitrate (NO3-) 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 NO3-, 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 NO3- (i.e., 0, 50, 200, 400 mg/L of NO3--N) for a 60-day period. The results indicated that increased exposure to NO3- (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 NO3-caused fluctuations in the plasma immune system. Higher exposure to NO3- (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, NO3- exposure resulted in upregulation of liver TNF-α, IL-1ß, HSP70, HSP90, and LYS. Additionally, the results suggested that NO3-exposure 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 NO3--N treatments. Finally, the results obtained from the analysis of the integrated biological responses version 2 (IBRv2) also confirmed the toxic effects of NO3- on juvenile turbot. According to these findings, it can be found that NO3- emission in the aquatic environment needs to be strictly controlled, as it may cause immune and lipid metabolism disorders in fish.
