Transcriptome analysis reveals hepatotoxicity in zebrafish induced by cyhalofop‑butyl.

• Cyhalofop‑butyl caused liver damage and liver atrophy in zebrafish larvae. • Cyhalofop‑butyl affected liver function by increasing the activities of ALT and AST. • Cyhalofop‑butyl disturbed the lipid metabolism of liver in zebrafish via inhibition TG levels. • Cyhalofop‑butyl affected liver development by alteration of expressions of related genes. • Cyhalofop‑butyl induced metabolism and immune system disturbance at transcriptional levels. Cyhalofop‑butyl is a highly effective aryloxyphenoxypropionate herbicide and widely used for weed control in paddy fields. With the increasing residue of cyhalofop‑butyl, it poses a threat to the survival of aquatic organisms. Here, we investigated the effect of cyhalofop‑butyl on zebrafish to explore its potential hepatotoxic mechanism. The results showed that cyhalofop‑butyl induced hepatocyte degeneration, vacuolation and necrosis of larvae after embryonic exposure for 4 days and caused liver atrophy after 5 days. Meanwhile, the activities of enzymes related to liver function were significantly increased by 0.2 mg/L cyhalofop‑butyl and higher, such as alanine transaminase (ALT) and aspartate transaminase (AST). And the contents of triglyceride (TG) involved in lipid metabolism were significantly decreased by 0.4 mg/L cyhalofop-buty. The expression of genes related to liver development was also significantly down-regulated. Furthermore, transcriptome results showed that the pathways involved in metabolism, immune system and endocrine system were significantly impacted, which may be related to hepatoxicity. To sum up, the present study demonstrated the hepatoxicity caused by cyhalofop-buty and its underlying mechanism. The results may provide new insights for the risk of cyhalofop‑butyl to aquatic organisms and new horizons for the pathogenesis of hepatotoxicity. [ABSTRACT FROM AUTHOR]