Abstract

Despite the broad knowledge of copper-induced stress and toxicity, data on the physiological responses to acute copper exposure and the correlation of those activities to a generalized stress response are still limited. The present study aimed to assess the physiological responses of golden trout to overcome copper stress at concentrations of 60µg/L and 120µg/L after 96h, respectively. The activities of glucose-6-phosphate dehydrogenase (G6PD) phosphoenolpyruvate carboxykinase (PEPCK) and NADPH/NADP+ ratio were significantly increased, and metabolites including glucose 6-phosphate, fructose 1-phosphate and fatty acids significantly accumulated in fish liver, indicating that gluconeogenesis, the pentose-phosphate pathway, as well as alteration of the membrane fatty acid composition were activated to serve as a defense mechanism against 60µg/L of copper after 96h. After exposure to 120µg/L of copper for 96h, the NAD+ and ATP contents, the activities of enzymes in the glycolytic pathway (phosphofructokinase, PFK and pyruvate kinase, PK) and mitochondrial respiratory chain complex I decreased significantly in fish liver. In addition, carbohydrates and MDA accumulated in golden trout after 120µg/L copper treatment. These results indicated that 120µg/L of copper exposure may induce a metabolic stress in golden trout after 96h. The multi-marker approach allows us to reach a greater understanding of the effects of copper on physiological responses of golden trout.

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