Elevated temperature and PCO2 shift metabolic pathways in differentially oxidative tissues of Notothenia rossii

• Published in: Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology
• Main Authors: Strobel, Anneli, Leo, Elettra, Pörtner, Hans-Otto, Mark, Felix Christopher
• Format: Article in Journal/Newspaper
• Language: unknown
• Published: 2013
• Subjects: Antarctic; The Antarctic; Antarc*; Notothenia rossii
• Online Access: https://epic.awi.de/id/eprint/33385/; https://epic.awi.de/id/eprint/33385/1/Strobel2013b.pdf; https://doi.org/10.1016/j.cbpb.2013.06.006; https://hdl.handle.net/10013/epic.41861; https://hdl.handle.net/10013/epic.41861.d001

Mitochondrial plasticity plays a central role in setting the capacity for acclimation of aerobic metabolism in ectotherms in response to environmental changes. We still lack a clear picture if and to what extent the energy metabolism and mitochondrial enzymes of Antarctic fish can compensate for changing temperatures or PCO2 and whether capacities for compensation differ between tissues. We therefore measured activities of key mitochondrial enzymes (citrate synthase (CS), cytochrome c oxidase (COX)) from heart, red muscle, white muscle and liver in the Antarctic fish Notothenia rossii after warm- (7 degrees C) and hypercapnia- (0.2kPa CO2) acclimation vs. control conditions (1 degrees C, 0.04kPa CO2). In heart, enzymes showed elevated activities after cold-hypercapnia acclimation, and a warm-acclimation-induced upward shift in thermal optima. The strongest increase in enzyme activities in response to hypercapnia occurred in red muscle. In white muscle, enzyme activities were temperature-compensated. CS activity in liver decreased after warm-normocapnia acclimation (temperature-compensation), while COX activities were lower after cold- and warm-hypercapnia exposure, but increased after warm-normocapnia acclimation. In conclusion, warm-acclimated N. rossii display low thermal compensation in response to rising energy demand in highly aerobic tissues, such as heart and red muscle. Chronic environmental hypercapnia elicits increased enzyme activities in these tissues, possibly to compensate for an elevated energy demand for acid-base regulation or a compromised mitochondrial metabolism, that is predicted to occur in response to hypercapnia exposure. This might be supported by enhanced metabolisation of liver energy stores. These patterns reflect a limited capacity of N. rossii to reorganise energy metabolism in response to rising temperature and PCO2.