College of Sciences, China Agricultural University, Beijing, China.
Risk Assessment Laboratory for Bee Products Quality and Safety of Ministry of Agriculture, Institute of Agricultural Research, Chinese Academy of Agricultural Sciences, Beijing, 100093, China.
Environ Pollut. 2019 Apr;247:775-782. doi: 10.1016/j.envpol.2019.01.054. Epub 2019 Jan 18.
Boscalid as one of the most widely used succinate dehydrogenase inhibitor (SDHI) fungicides has been frequently detected in both freshwater and estuarine environments. Its acute toxic effects on zebrafish and freshwater algae have been reported in our previous studies. To further investigate its chronic toxic effects to aquatic organisms, adult zebrafish were exposed for 28 days to a series of environmentally relevant boscalid concentrations in this study. Growth indicators and histopathology were determined in this study. Results indicated that boscalid inhibited the growth of zebrafish and induced damage in the kidneys and liver. Carbohydrate and lipid metabolism as the key pathways of energy metabolism in growth of zebrafish were also investigated. Results showed boscalid caused an increase in the activity of hexokinase (HK), the content of glycogen, glucose-6-phosphatase (G6Pase), and insulin (INS) in liver and a decrease in blood glucose content and succinate dehydrogenase (SDH) activity. Boscalid reduced the total content of triacylglyceride (TG) and cholesterol (TC) and the activity of fatty acid synthase (FAS) and acetyl coenzyme A carboxylase (ACC) in the liver. Correspondingly, expression of the genes related to carbohydrate and lipid metabolism in liver and intestine was affected by boscalid, especially in the significant upregulation of G6Pase and pparα and downregulation of SGLT-1 and AMY. Results suggested that boscalid could affect carbohydrate metabolism of adult zebrafish via regulation of gluconeogenesis and glycolysis at 0.1 mg/L. Moreover, boscalid might induce an increase in β-oxidation and a decrease in lipid synthesis at 0.01 mg/L. In conclusion, our study identified that carbohydrate and lipid metabolism are the possible biological pathways that mediate boscalid-induced developmental effects.
波尔多酸作为最广泛使用的琥珀酸脱氢酶抑制剂 (SDHI) 类杀菌剂之一，已在淡水和河口环境中频繁检出。在我们之前的研究中，已经报道了其对斑马鱼和淡水藻类的急性毒性作用。为了进一步研究其对水生生物的慢性毒性作用，本研究中成年斑马鱼在一系列环境相关的波尔多酸浓度下暴露 28 天。本研究测定了生长指标和组织病理学变化。结果表明，波尔多酸抑制了斑马鱼的生长，并导致其肾脏和肝脏受损。还研究了碳水化合物和脂质代谢作为斑马鱼生长中能量代谢的关键途径。结果表明，波尔多酸导致肝脏中己糖激酶 (HK) 活性、糖原含量、葡萄糖-6-磷酸酶 (G6Pase) 和胰岛素 (INS) 含量增加，血糖含量和琥珀酸脱氢酶 (SDH) 活性降低。波尔多酸降低了肝脏中三酰甘油 (TG) 和胆固醇 (TC) 的总含量以及脂肪酸合成酶 (FAS) 和乙酰辅酶 A 羧化酶 (ACC) 的活性。相应地，肝脏和肠道中与碳水化合物和脂质代谢相关的基因表达受到波尔多酸的影响，特别是 G6Pase 和 pparα 的显著上调以及 SGLT-1 和 AMY 的下调。结果表明，波尔多酸可以通过调节 0.1mg/L 时的糖异生和糖酵解来影响成年斑马鱼的碳水化合物代谢。此外，波尔多酸可能在 0.01mg/L 时诱导β-氧化增加和脂质合成减少。总之，本研究确定了碳水化合物和脂质代谢是介导波尔多酸诱导发育效应的可能生物学途径。
