Analysis of the Biochemical Effect of Enrofloxacin on American Shad (Alosa sapidissima) Infected with Aeromonas hydrophila

In order to find the biochemical effects of <i>Aeromonas hydrophila</i> and its therapeutic chemical, enrofloxacin (ENR), on American shad (<i>Alosa sapidissima</i> A. Wilson), four groups were set up: a control group (C), an <i>A. hydrophila</i> group (A), an <i>A. hydrophila</i> + 70 mg·L^-1 enrofloxacin (ENR) group (E1), and an <i>A. hydrophila</i> + 140 mg·L^-1 ENR group (E2). Histological, enzymatic activities, transcriptome, and proteomics have been performed. MDA, PPO, AKP, TNF-α, and AMPK were significantly increased, while AhR and EROD were decreased in the liver of American shad after treatment with <i>A. hydrophila</i>. AhR and EROD showed a significant decrease in E1 group; MDA, PPO, AKP, and AMPK were significantly increased, while AhR and EROD decreased in E2 group. <i>A. hydrophila</i> significantly increased ferroptosis, TGF-β signaling pathway, etc. Ferroptosis, pyrimidine metabolism, and glycerolipid metabolism significantly increased in E1 group, while protein processing in endoplasmic reticulum significantly increased in E2 group. A total of 126 shared metabolites were found in the comparisons of A vs. C and E2 vs. C, and the main enriched pathway were organic oxygen compounds, lipids, and lipid-like molecules. Except for fluorobenzoate degradation, the pathways of ascorbate and aldarate metabolism, pyrimidine metabolism significantly increased in A and E2 groups, which further resulted in vacuolization, cell shedding, and necrosis in the liver. <i>A. hydrophila</i> led to a significant decrease in lipid metabolism, leading to oxidative stress and energy expenditure. The addition of ENR in aquaculture significantly enhanced liver metabolic abnormalities caused by <i>A. hydrophila</i>. Excessive use of ENR leads to oxidative stress in American shad, affecting its immune system as well as lipid, carbohydrate, and energy metabolism.