Waterborne zinc mitigates cadmium-induced toxicity in the mud crab (Scylla paramamosain) through regulation of bioaccumulation, oxidative stress, and lipid metabolism.

This study assessed the protective effects of zinc (Zn) against cadmium (Cd) toxicity in mud crabs, focusing on metal accumulation, tissue damage, antioxidant responses, fatty acid composition, and gene expression. Cd exposure resulted in significantly elevated metal concentrations, predominantly in the hepatopancreas, followed by gills and muscle tissues (P < 0.05). Co-exposure with Zn markedly reduced Cd accumulation, especially in the hepatopancreas and gills (P < 0.05), indicating a competitive or regulatory interaction between the two metals. Histological examination revealed severe tissue damage in Cd-exposed crabs, characterized by necrosis and epithelial detachment, whereas Zn supplementation substantially mitigated these pathological changes and preserved tissue integrity. Cadmium exposure disrupted antioxidant homeostasis, notably reducing catalase (CAT) activity in the hepatopancreas (P < 0.05). In contrast, Zn co-treatment enhanced antioxidant capacity, as evidenced by increased CAT activity and glutathione (GSH) levels in both hepatopancreas and gill tissues (P < 0.05). Lipid metabolism was also adversely affected by Cd, with significant reductions in total fatty acids, saturated fatty acids (SFA), and monounsaturated fatty acids (MUFA) (P < 0.05). Notably, Zn supplementation restored these lipid fractions, with a pronounced recovery of omega-3 fatty acids (P < 0.05), suggesting improved metabolic resilience. Furthermore, gene expression analysis indicated that Cd exposure upregulated genes associated with lipid metabolism (P < 0.05), whereas Zn co-exposure moderated these transcriptional changes (P < 0.05). These findings show that waterborne Zn mitigates Cd toxicity in mud crabs by reducing metal accumulation, preserving tissue integrity, and improving antioxidant and metabolic responses.