In order to find the biochemical effects of Aeromonas hydrophila and its therapeutic chemical, enrofloxacin (ENR), on American shad (Alosa sapidissima A. Wilson), four groups were set up: a control group (C), an A. hydrophila group (A), an A. hydrophila + 70 mg·L−1 enrofloxacin (ENR) group (E1), and an A. hydrophila + 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 A. hydrophila. 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. A. hydrophila 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. A. hydrophila 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 A. hydrophila. Excessive use of ENR leads to oxidative stress in American shad, affecting its immune system as well as lipid, carbohydrate, and energy metabolism.
Zheng et al. (Mon,) studied this question.
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