Most toxicity studies of prometryn in non-target aquatic animals have focused on hepatotoxicity, cardiotoxicity, embryonic developmental and growth toxicity, while studies on the molecular mechanisms of intestinal toxicity of prometryn are still unknown. In the current study, the intestinal tissues of the Chinese mitten crab (Eriocheir sinensis) were used to uncover the underlying molecular mechanisms of stress by 96-h acute in vivo exposure to prometryn. The results showed that prometryn activated the Nrf2-Keap1 pathway and up-regulated the expression of downstream antioxidant genes. Prometryn induced the expression of genes associated with non-specific immunity and autophagy, and induced apoptosis through the MAPK pathway. Interestingly, the significant up-or down-regulation of the above genes mainly occurred at 12 h- 24 h after exposure. Intestinal flora sequencing revealed that prometryn disrupted the intestinal normal barrier function mainly by reducing beneficial bacteria abundance, which further weakened the intestinal resistance to exogenous toxicants and caused an inflammatory response. Correlation analyses found that differential flora at the genus level had potential associations with gut stress-related genes. In conclusion, our study contributes to understanding the molecular mechanisms behind the intestinal stress caused by herbicides on aquatic crustaceans.
Keywords: Chinese mitten crab; Gut diseases; Immune response; Microbial flora; Triazines.
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