Effects of copper exposure and recovery in juvenile yellowtail kingfish (Seriola lalandi): Histological, physiological and molecular responses

• Published in: Aquaculture reports Vol. 31; p. 101669
• Main Authors: Jin, Zhixin, Xu, Yongjiang, Zhou, Heting, Cui, Aijun, Jiang, Yan, Wang, Bin, Zhang, Wenjing
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.08.2023; Elsevier
• Subjects: alanine transaminase; aquaculture; aspartate transaminase; blood serum; copper; Copper ecotoxicity; copper sulfate; disease control; Enzymatic activity; gene expression regulation; genes; glutathione peroxidase; histology; Histopathology; juveniles; lipid metabolism; liver; lysozyme; malondialdehyde; oxidative phosphorylation; Seriola lalandi; species; superoxide dismutase; toxicity; Transcriptome analysis; Copper ecotoxicity; Transcriptome analysis; Histopathology; Enzymatic activity; Seriola lalandi
• ISSN: 2352-5134; 2352-5134
• DOI: 10.1016/j.aqrep.2023.101669

This study investigated the physiological responses to copper toxicity in liver and gill of juvenile yellowtail kingfish by exposing to 0 (control), 0.0672, 0.12, 0.214, 0.384, 0.672, 1.20, or 2.14 mg/L copper sulfate for 7 days and then recovered for 14 days. The histopathology, enzyme activities and differential gene expression were detected. The results indicate the safe concentration value of copper for juvenile yellowtail kingfish is 0.083 mg/L. Copper exposure caused structural damage to gill and liver, and could be disappeared or restored after the recovery period. Copper exposure enhanced the Cu,Zn superoxide dismutase (Cu/Zn-SOD) and glutathione peroxidase (GSH-Px) activities and the malondialdehyde (MDA) level in liver. However, with increasing copper concentrations, liver aspartate transaminase (AST) and gill Na+/K+-ATPase activities were at first enhanced and then inhibited. Serum lysozyme (LZM) and Cu/Zn-SOD activities were enhanced at low copper concentrations but inhibited at high concentrations, and the activities of alanine transaminase (ALT) and AST significantly increased at greater copper concentrations. After the recovery period, only liver Cu/Zn-SOD activity returned to control level. In contrast, liver GSH-Px activity and MDA levels and gill Na+/K+-ATPase activity, serum LZM and AST activities remained significantly higher than control, but liver AST activity, serum ALT, and Cu/Zn-SOD activities were significantly lower than control. We constructed the gene regulatory networks of molecular pathways in liver and gill in response to copper exposure. The DEGs were enriched mainly in the pathway of lipid metabolism in liver and pathway of oxidative phosphorylation in gill, indicating these respective pathways are involved in the response to copper stress in this species. The present results elucidate some histological, physiological, and molecular mechanisms underlying copper-exposure stresses in yellowtail kingfish, which could help guide the safe utilization of copper sulfate in disease control of farmed individuals. •The 96 h-LC50 and the SC values of copper sulfate were determined for juvenile yellowtail kingfish.•Copper exposure caused adverse impairment in liver and gill, which could be restored after recovery.•Immune-related enzymes could be used as biomarkers for evaluating copper stress in yellowtail kingfish.•Lipid metabolism and oxidative phosphorylation were mainly involved in copper stress resistance in yellowtail kingfish.