Influences of chronic copper exposure on intestinal histology, antioxidative and immune status, and transcriptomic response in freshwater grouper (Acrossocheilus fasciatus).

Copper (Cu) contamination is commonly found in both natural water environments and fish farms, and it can cause severe damage to different fish organs, but Cu-induced intestinal damage has been rarely studied. This study subjected three groups of freshwater grouper (Acrossocheilus fasciatus) (initial weight: 1.56 ± 0.10 g) to 0 mg/L, 0.01 mg/L, and 0.04 mg/L Cu2+ for 30 days, named Con, Cu0.01, and Cu0.04 groups, respectively. The histological observation indicated that the Cu0.04 group caused a significant decrease in villus length, lamina propria width, and muscular thickness compared to the Con group (P < 0.05). Additionally, the Cu0.04 group significantly increased intestinal superoxide dismutase (SOD), glutathione peroxidase (GPx), lysozyme (LZM) activities, as well as malondialdehyde (MDA) content than the Con group (P < 0.05). Meanwhile, the Cu0.01 and Cu0.04 groups showed significantly increased immunoglobulin M (IgM), complement 3 (C3), and glutathione (GSH) contents than the Con group (P < 0.05). Transcriptomic analysis revealed a total of 101 differentially expressed genes (DEGs), including 47 up-regulated and 54 down-regulated DEGs, were identified between the Cu0.04 and Con groups. Notably, the DEGs were mainly related to intestinal structure construction, immune functions, apoptosis, and resistance to DNA damage and pathogen infection. The findings suggest that chronic Cu exposure caused intestinal histological alterations, activated the antioxidative and immune systems, and induced systematic adaptation to cope with the physical barrier injury, DNA damage, and potential pathogen growth. • 0.04 mg/kg Cu2+ caused a decrease in intestinal villus length, lamina propria width, and muscular thickness. • Cu2+ exposure activated the intestinal antioxidative and non-specific immune systems. • Intestinal structure construction, immunity, apoptosis, and resistance to DNA damage were activated by Cu2+ exposure. [ABSTRACT FROM AUTHOR]