Integration of transcriptomics, gut microbiota, and physiology reveals the toxic response of bensulfuron-methyl in Procambarus clarkii

Bensulfuron-methyl (BSM) enters the environment through agricultural practices, posing a threat to the health of aquatic organisms. Currently, the toxic mechanisms of BSM on crayfish (Procambarus clarkii) have not been thoroughly investigated. In this study, crayfish were exposed to BSM solutions at concentrations of 0, 5, and 10 mg/L for 48 h. The study integrated physiological, gut microbiota, and transcriptomic analyses to investigate the mechanisms of action. BSM exposure induced oxidative stress responses in crayfish, resulting in changes in superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSH) activity, and malondialdehyde (MDA) levels. Exposure to BSM caused damage to the intestinal tissues, reduced gut microbiota diversity, increased the abundance of harmful bacteria, and led to intestinal dysfunction. Analysis of the hepatopancreas revealed significant tissue damage. Transcriptomic data indicated that BSM affects the growth of crayfish through genes related to immune response (SLC17A5, CTSD, CTSB, NFKBIA, Mincle). The lysosomal pathway and NF-κB pathway were notably affected. This study analyzed the negative impacts of BSM on crayfish from various levels and provided detailed data to enhance our understanding of the toxic mechanisms of BSM in aquatic organisms. [Display omitted] •Bensulfuron-methyl induces oxidative stress responses in red swamp crayfish.•Bensulfuron-methyl causes histological damage to the gut of red swamp crayfish.•Bensulfuron-methyl causes damage to the hepatopancreas of red swamp crayfish.•Bensulfuron-methyl alters the gut microbiota in red swamp crayfish.•Immune-related genes influenced in changes to the lysosomal and NF-κB pathways.