Abstract
Prometryn is commonly used in agricultural and non-agricultural settings. However, possible harm to aquatic organisms remains a persistent concern. Prometryn was also the only one of the 26 triazine herbicides detected in this study. Numerous studies have assessed the harmful effects of prometryn in teleost fish and shrimp. There is a lack of information regarding the ecological and human health risks, as well as the toxic mechanisms affecting crayfish. In this study, human health risk assessment (THQ) and ecological risk assessment (RQ) were conducted on P. clarkii in the rice-crayfish co-culture (IRCC) farming model. The 96 h of exposure to 0.286 mg/L and 1.43 mg/L prometryn was conducted to investigate the potential effects and molecular mechanisms of hepatopancreatic resistance to prometryn in P. clarkii. The original sample analysis revealed that the THQ calculated from the prometryn levels in the muscle and hepatopancreas was below 0.1, suggesting no threat to human health. However, the calculated RQ values were >0.1, indicating a risk to P. clarkii. Histological analysis and biochemical index detection of the experimental samples revealed that the hepatopancreatic injury and oxidative damage in P. clarkii were caused by prometryn. Moreover, transcriptome analysis identified 2512 differentially expressed genes (DEGs) after 96 h of prometryn exposure. Prometryn exposure caused significant changes in metabolic pathways, including oxoacid metabolic processes and cytochrome P450-associated drug metabolism. Further hub gene analysis via PPI indicated that exposure to prometryn may inhibit lipid synthesis, storage, and amino acid transport and affect glucose metabolic pathways and hormone synthesis. Additionally, we hypothesized that prometryn-triggered cell death could be linked to the PI3K-Akt signaling cascade. This study's findings have significant meaning for the efficient and logical application of herbicides in IRCC, ultimately aiding in advancing a highly productive agricultural system.
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