Metabolic responses of golden trout (Oncorhynchus mykiss aguabonita) after acute exposure to waterborne copper

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 60 mu g/L and 120 mu g/L after 96 h, 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 60 mu g/L of copper after 96 h. After exposure to 120 mu g/L of copper for 96 h, 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 120 mu g/L copper treatment. These results indicated that 120 mu g/L of copper exposure may induce a metabolic stress in golden trout after 96 h. The multi-marker approach allows us to reach a greater understanding of the effects of copper on physiological responses of golden trout.

Automated summary

This study aimed to evaluate the physiological responses of golden trout to acute copper exposure. The results showed that at a concentration of 60 µg/L, the fish exhibited gluconeogenesis, pentose-phosphate pathway activation, and alteration of fatty acid composition in response to copper exposure. At a concentration of 120 µg/L, the fish showed signs of metabolic stress.