Fenazaquin impairs liver development and metabolic homeostasis in zebrafish (Danio rerio) by disrupting glucose and lipid metabolism.

Fenazaquin (FEN) is an emerging low-dose acaricide used for mite control in vegetable crops. It is potential to enter aquatic environments via runoff, yet studies on its toxicity to aquatic organisms remain limited. This study aims to assess the harmful impact of FEN on the liver, with zebrafish serving as the animal model. FEN triggered developmental toxicity and impaired liver development in zebrafish embryos, along with liver injury in adults. Remarkably, F1 offspring that were never directly exposed to FEN still exhibited deficits in growth and development. In zebrafish embryos, FEN exposure led to reduced hepatic lipid accumulation, whereas in adult zebrafish liver, FEN promoted lipid deposition. FEN also increased the enzymatic activities of alanine transaminase and aspartate aminotransferase, alter total cholesterol and triglycerides contents in zebrafish embryos and adult zebrafish livers, and disrupt lipid and carbohydrate metabolism in adult zebrafish livers. Furthermore, qRT-PCR analysis revealed that FEN altered the expressions of genes related to growth and development, fatty acid, sterol, steroid, glyceride, carbohydrate metabolism. Transcriptomic analysis of embryos revealed extensive remodeling of lipid and carbohydrate metabolic pathways in embryos. Therefore, FEN may impair liver development and metabolic homeostasis by disrupting glucose and lipid metabolism in zebrafish.