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.
Keywords: Boscalid; Carbohydrate metabolism; Lipid metabolism; Zebrafish; β-Oxidation.
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