Abstract

Pyraclostrobin (PY) is highly toxic to aquatic organisms, and its increased residues in aquatic environments may have harmful effects on the intestine of aquatic creatures. Previous research demonstrated that vitamin E (VE) alleviated the acute toxicity of PY to zebrafish. This study further explored the mitigation effect of VE on PY-induced intestinal toxicity in fish and the underlying mechanisms by exposing adult zebrafish to PY (10, 20 μg/L) with or without 4 μM VE supplementation for 21 days. The results showed that VE alleviated the gut histopathological lesions caused by PY. VE co-exposure also improved PY-induced intestinal inflammation and restored the expression level of genes encoding intestinal tight junction protein. Furthermore, VE restored the anti-oxidation level inhibited by PY and reduced pro-apoptotic cytokine level and apoptotic enzyme activity increased by PY. 16S rRNA high-throughput sequencing showed that VE improved the zebrafish intestinal flora imbalance caused by 20 μg/L PY, increased the relative abundance of beneficial bacterium Cetobacterium, and reduced the relative abundance of pathogenic bacteria. In conclusion, VE alleviated PY-induced intestinal toxicity via repairing the damaged intestinal mucosal barrier, inhibiting inflammation, reducing oxidative stress and apoptosis, and improving the intestinal microbial disorder in zebrafish.

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