CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, PR China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, 7 Nanhai Road, Qingdao, 266071, PR China; Center for Ocean Mega-Science, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, PR China; University of Chinese Academy of Sciences, Beijing, China.
CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, PR China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, 7 Nanhai Road, Qingdao, 266071, PR China; Center for Ocean Mega-Science, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, PR China.
Environ Pollut. 2021 Aug 15;283:117103. doi: 10.1016/j.envpol.2021.117103. Epub 2021 Apr 14.
Nitrate (NO) is one of the common inorganic nitrogen compound pollutants in natural ecosystems, which may have serious risks for aquatic organisms. However, its toxicological mechanism remains unclear. In the current study, juvenile turbot (Scophthalmus maximus) were exposed to different concentrations of NO (CK- 3.57 ± 0.16, LN - 60.80 ± 1.21, MN - 203.13 ± 10.97 and HN - 414.16 ± 15.22 mg/L NO-N) for 60 d. The blood biochemical assays results revealed that elevated NO exposure significantly increased the concentrations of plasma NO, NO, MetHb, K, cortisol, glucose, triglyceride, lactate, while significantly decreased the concentrations of plasma Hb, Na and Cl, which meant that NO caused hypoxic stress and further affected the osmoregulation and metabolism in fish. Besides, exposure to MN and HN induced a significant decrease in the level of antioxidants, including SOD (Point: 60th day, MN, HN v.s. CK: 258.36, 203.73 v.s. 326.95 U/mL), CAT (1.97, 1.17 v.s. 2.37 U/mL), GSH (25.38, 20.74 v.s. 37.00 μmol/L), and GPx (85.32, 71.46 v.s. 129.36 U/mL), and a significant increase of MDA (7.54, 9.73 v.s. 5.27 nmol/L), suggesting that NO exposure leading to a disruption of the redox status in fish. Also, further research revealed that NO exposure altered the mRNA levels of p53 (HN: up to 4.28 folds) and p53-regulated downstream genes such as Bcl-2 (inferior to 0.44 folds), caspase-3 (up to 2.90 folds) and caspase-7 (up to 3.49 folds), indicating that NO exposure induced abnormal apoptosis in the fish gills. Moreover, IBRv2 analysis showed that the toxicity of NO exposure to turbot was dose-dependent, and the toxicity peaked on the 15th day. In short, NO is an environmental toxicological factor that cannot be ignored, because its toxic effects are long-term and could cause irreversible damage to fish. These results would be beneficial to improve our understanding of the toxicity mechanism of NO to fish, which provides baseline evidence for the risk assessment of environmental NO in aquatic ecosystems.
硝酸盐（NO）是自然生态系统中常见的无机氮化合物污染物之一，可能对水生生物造成严重风险。然而，其毒理学机制尚不清楚。在本研究中，将大菱鲆幼鱼（Scophthalmus maximus）暴露于不同浓度的硝酸盐（CK-3.57±0.16、LN-60.80±1.21、MN-203.13±10.97 和 HN-414.16±15.22 mg/L 的 NO-N）中 60 天。血液生化分析结果表明，升高的 NO 暴露显著增加了血浆 NO、NO、MetHb、K、皮质醇、葡萄糖、甘油三酯、乳酸的浓度，而显著降低了血浆 Hb、Na 和 Cl 的浓度，这意味着 NO 引起了缺氧应激，并进一步影响了鱼类的渗透压和代谢。此外，MN 和 HN 的暴露导致抗氧化剂水平显著下降，包括 SOD（第 60 天，MN、HN 与 CK 相比：258.36、203.73 与 326.95 U/mL）、CAT（1.97、1.17 与 2.37 U/mL）、GSH（25.38、20.74 与 37.00 μmol/L）和 GPx（85.32、71.46 与 129.36 U/mL），而 MDA（7.54、9.73 与 5.27 nmol/L）显著增加，表明 NO 暴露导致鱼类氧化还原状态失衡。此外，进一步的研究表明，NO 暴露改变了 p53（HN：增加到 4.28 倍）和 p53 调节的下游基因（如 Bcl-2（降低到 0.44 倍）、caspase-3（增加到 2.90 倍）和 caspase-7（增加到 3.49 倍）的 mRNA 水平，表明 NO 暴露诱导了鱼类鳃的异常细胞凋亡。此外，IBRv2 分析表明，NO 暴露对大菱鲆的毒性是剂量依赖性的，毒性在第 15 天达到峰值。总之，NO 是一个不可忽视的环境毒理学因素，因为它的毒性作用是长期的，可能会对鱼类造成不可逆转的损害。这些结果将有助于提高我们对 NO 对鱼类毒性机制的认识，为水生生态系统中环境 NO 的风险评估提供基础证据。
