Multi-system toxicity of lead (Pb) in Procambarus clarkii: Integrated analysis of tissue damage, immune dysfunction, oxidative stress, and microbial dysbiosis via multi-omics approaches.

The element lead (Pb) exhibits significant toxicity throughout aquatic habitats. Crustaceans sit at the top of the aquatic food chain and therefore are especially susceptible to Pb-associated toxicity. Nevertheless, there is limited information on the crustaceans exposed to Pb. Hence, in this study, the acute Pb-mediated alterations of histopathology, hepatopancreas transcriptome, and gut microbiomes of Procambarus clarkii (P. clarkii) were performed. Pb exposure caused hepatopancreas damage (lumen dilatation, epithelial vacuolization) and intestinal lesions (disrupted lamina propria and epithelium). RNA-seq revealed differentially expressed genes (DEGs) in the hepatopancreas, including immune-related (PGRMC1, TAK1, CDC42, USP2), oxidation-reduction-related (XDH, G6PD, CYP4C1, CYP6K1, CYP9E2), and ion transport genes (TNC2, LETM1, ABCA1/3/10), suggesting Pb disrupts immunity, oxidation-reduction balance, and ion homeostasis. Additionally, examination of the bacterial 16S rRNA gene demonstrated that Pb induced a significantly reduction in both the diversity and abundance of bacteria, resulting in a notable perturbation in the composition of the gut microbiome. The exposure to Pb resulted in significant alterations in 4 phyla and 13 genera. The findings indicated that the presence of Pb might impede the capacity to synthesis of amylases, glucose assimilation, chitin degradation, and antibacterial activity. Taken together, the results of our study provided insights into the multiple mechanisms underlying Pb toxicity in aquatic crustaceans, encompassing tissue, cellular, molecular, and microbial levels.