Evaluation of the combined effects of manganese and thermal stress on the metabolic capacities of Arctic charr (Salvelinus alpinus)

In Northern Canada, pollution from mining discharges represents a significant environmental stressor for aquatic organisms. Variations in water temperature constitute another source of stress for fish. Although numerous studies have investigated the effects of environmental stressors on fish physiology, research specifically addressing their impact on energy metabolism pathways remains limited. In this study, we investigated the effects of manganese (Mn), thermal acclimation, and their combination on cellular energy metabolism pathways in Arctic charr, a cold-water stenotherm. Juvenile charr were acclimatized to two contrasting temperatures (7 degrees C and 16 degrees C) for two weeks. Thereafter, half of the specimens where exposed to Mn (1 mg/L) for eight weeks. After 56 days, mortality was higher in fish acclimatized to 16 degrees C compared to 7 degrees C. Trace metal analysis performed by ICP-AES showed that bioaccumulation of Mn in gills and kidney was higher at 7 degrees C than at 16 degrees C, while the bioaccumulation of Mn in liver and muscle was not affected by temperature. Enzyme assays performed in liver and muscle showed a decrease in aerobic capacity and an increase in glycolytic capacity caused by Mn combined with a high temperature. Hepatic cytochrome C oxidase activity was significantly lower in fish acclimatized at 16 degrees C and exposed to Mn compared to other treatments. Hepatic citrate synthase activity showed a decrease in fish from the 16 degrees C and Mn treatment compared to those at 7 degrees C without Mn exposure. In both tissues, phosphofructokinase activity increased in fish acclimatized at 16 degrees C and exposed to Mn compared to both treatments at 7 degrees C. Hepatic lactate dehydrogenase activity was lower at 16 degrees C than at 7 degrees C in fish from the control treatment. The activity of beta-hydroxyacyl-CoA dehydrogenase was unaffected by temperature or Mn. These results suggest that Mn, combined with high temperature, may affect mitochondrial function leading to a decrease in aerobic capacity. In response to the decline of cellular respiration capacity, metabolic pathways responded differently. Aerobic glycolysis was stimulated, while lipid metabolism showed no metabolic adjustment. This study represents one of the first steps towards understanding Mn toxicity in the context of climate change in a cold-water stenothermic species, and its impact on fish health and metabolism.