Acute cadmium exposure induced intestinal barrier damage in the hybrid grouper (Epinephelus fuscoguttatus♂ × Epinephelus lanceolatus♀)

Cadmium (Cd), a widespread aquatic pollutant, induces dose-dependent gill epithelial damage in hybrid grouper (Epinephelus fuscoguttatus × Epinephelus lanceolatus). However, the toxicological mechanisms underlying its effects on intestinal mucosal barrier function remain unclear. This study examined intestinal mucosal barrier injury in hybrid grouper exposed to three Cd concentrations: 0 mg/L (control, CON), 0.0363 mg/L (Cd1%), and 0.363 mg/L (Cd10%). Cd exposure significantly inhibited intestinal trypsin and lipase activities compared with the control group. In addition, Cd exposure reduced villus height and muscularis propria thickness, disrupted tight junction structures, and induced mitochondrial vacuolization. Cd exposure also significantly downregulated the expression of occludin1, ZO-1, and claudin7a. Compared to the control group, the Cd10% group showed fewer intestinal goblet cells, accompanied by mitochondrial calcium deposition. Analysis of the intestinal microbiota revealed that Cd exposure significantly decreased the diversity of the intestinal microbiota. Specifically, compared with the control group, Cd exposure significantly increased the relative abundance of Pseudomonadota, while concurrently decreasing the relative abundances of Bacteroidota and Bacillota. Additionally, Cd exposure reduced Prevotellaceae (including Prevotella ruminicola) but increased Vibrionaceae (particularly Vibrio and V. vulnificus CMCP6). Functional prediction analysis revealed that Cd exposure significantly suppressed the digestive system pathways in the intestinal microbiota. Intestinal gene expression analysis further showed that the Cd10% group exhibited downregulation of MHC, TGF, and NRF2 and upregulation of IL-1β relative to the control group. In summary, Cd exposure impairs digestive function, induces structural damage to intestinal tissues, disrupts intestinal microbiota homeostasis, compromises intestinal barrier integrity, and elevates inflammation risk in hybrid grouper. The findings establish a theoretical framework for both ecological risk assessment of Cd exposure and sustainable practices in aquaculture. • Acute Cd exposure damaged intestinal villi structure and epithelial tight junctions. • Acute Cd exposure significantly inhibited intestinal trypsin and lipase activities in hybrid grouper. • Cd exposure induces intestinal microbiota dysbiosis, increasing intestinal inflammation susceptibility in hybrid grouper.