Hunan Fisheries Science Institute, Changsha 410153, China.
Genes (Basel). 2023 Dec 10;14(12):2196. doi: 10.3390/genes14122196.
Niclosamide (NIC, 2',5-dichloro-4'-nitrosalicylanilide) is a salicylanilide molluscicide, and the extensive utilization and environmental pollution associated with NIC engender a potential hazard to both human health and the wellbeing of aquatic organisms. However, the mechanism of the chronic toxicity of NIC at environmentally relevant concentrations in terms of oxidative stress, metabolic disorder, and barrier functions in black carp () is unknown. Therefore, healthy juvenile black carp () (average weight: 38.2 ± 2.5 g) were exposed to NIC at an environmentally realistic concentration (0, 10, and 50 μg/L) for 28 days. The findings of this study indicate that exposure to NIC resulted in reductions in weight gain, decreased activity of antioxidant enzymes, and increased expression of the Nrf2 gene. Furthermore, the liver demonstrated a greater accumulation of NIC than that in the gut and gills, as determined with a chemical analysis. Additionally, NIC exposure led to a significant reduction in ATP content and the activity of Na/K-ATPase and Ca/Mg-ATPase in the gut. Meanwhile, exposure to NIC resulted in a decrease in the liver glucose (Glu) level, gut cholesterol (CHO), and glycogen (Gln) and triglyceride (TG) content in all examined tissues. Conversely, it led to an increase in tissue lactic acid (LA) and acetyl-CoA levels, as well as LDH activity. Furthermore, NIC exposure at environmentally relevant concentrations demonstrated an upregulation in the expression of genes associated with glycolysis, such as and , while concurrently downregulating the gluconeogenesis gene . Additionally, NIC exhibited an upregulation in the expression of genes related to -oxidation, such as and , while downregulating genes involved in triglyceride synthesis, including , , , and . Moreover, NIC facilitated fatty acid transportation through the overexpression of and . These results suggest that chronic exposure to NIC is associated with oxidative stress, compromised barrier function, and metabolic disorder. Moreover, these results underscore the significance of assessing the potential consequences of NIC for black carp and aquatic environments for aquaculture.
硝氯酚(NIC,2',5-二氯-4'-亚硝基苯甲酰胺)是一种杀螺剂,其广泛应用和环境污染对人类健康和水生生物的福利都构成了潜在威胁。然而,硝氯酚在环境相关浓度下对鱼类的慢性毒性机制,包括氧化应激、代谢紊乱和屏障功能,尚不清楚。因此,本研究选用健康的幼龄草鱼(平均体重:38.2 ± 2.5 g),在环境实际浓度(0、10 和 50 μg/L)下暴露于硝氯酚 28 天。研究结果表明,暴露于硝氯酚会导致体重增加减少、抗氧化酶活性降低、Nrf2 基因表达增加。此外,与肠道和鳃相比,肝脏中硝氯酚的积累量更大,这可以通过化学分析来确定。此外,暴露于硝氯酚会导致肠道中 ATP 含量和 Na/K-ATPase 和 Ca/Mg-ATPase 活性显著降低。同时,暴露于硝氯酚会导致肝脏葡萄糖(Glu)水平、肠道胆固醇(CHO)、糖原(Gln)和甘油三酯(TG)含量在所有检测组织中降低。相反,它会导致组织中乳酸(LA)和乙酰辅酶 A 水平以及 LDH 活性增加。此外,暴露于环境相关浓度的硝氯酚会导致与糖酵解相关的基因,如 和 ,表达上调,同时下调糖异生基因 。此外,硝氯酚还会上调与β-氧化相关的基因,如 和 ,同时下调参与甘油三酯合成的基因,包括 、 、 、和 。此外,硝氯酚通过过表达 和 促进脂肪酸的运输。这些结果表明,慢性暴露于硝氯酚会导致氧化应激、屏障功能受损和代谢紊乱。此外,这些结果强调了评估硝氯酚对草鱼和水产养殖环境的潜在影响的重要性。