title: Effects of increased CO2 on fish gill and plasma proteome.
abstract: Ocean acidification and warming are both primarily caused by increased levels of atmospheric CO2, and marine organisms are exposed to these two stressors simultaneously. Although the effects of temperature on fish have been investigated over the last century, the long-term effects of moderate CO2 exposure and the combination of both stressors are almost entirely unknown. A proteomics approach was used to assess the adverse physiological and biochemical changes that may occur from the exposure to these two environmental stressors. We analysed gills and blood plasma of Atlantic halibut (Hippoglossus hippoglossus) exposed to temperatures of 12 °C (control) and 18 °C (impaired growth) in combination with control (400 µatm) or high-CO2 water (1000 µatm) for 14 weeks. The proteomic analysis was performed using two-dimensional gel electrophoresis (2DE) followed by Nanoflow LC-MS/MS using a LTQ-Orbitrap. The high-CO2 treatment induced the up-regulation of immune system-related proteins, as indicated by the up-regulation of the plasma proteins complement component C3 and fibrinogen β chain precursor in both temperature treatments. Changes in gill proteome in the high-CO2 (18 °C) group were mostly related to increased energy metabolism proteins (ATP synthase, malate dehydrogenase, malate dehydrogenase thermostable, and fructose-1,6-bisphosphate aldolase), possibly coupled to a higher energy demand. Gills from fish exposed to high-CO2 at both temperature treatments showed changes in proteins associated with increased cellular turnover and apoptosis signalling (annexin 5, eukaryotic translation elongation factor 1γ, receptor for protein kinase C, and putative ribosomal protein S27). This study indicates that moderate CO2-driven acidification, alone and combined with high temperature, can elicit biochemical changes that may affect fish health.
authors: Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden.
authors: Karine
authors: K
authors: Bresolin de Souza
authors: Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden.
authors: Fredrik
authors: F
authors: Jutfelt
authors: Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden.
authors: Peter
authors: P
authors: Kling
authors: Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden.
authors: Lars
authors: L
authors: Förlin
authors: Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden.
authors: Joachim
authors: J
authors: Sturve
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D002245:Carbon Dioxide / Q000494:pharmacology*; D002853:Chromatography, Liquid; D003176:Complement C3 / Q000235:genetics / Q000378:metabolism; D004734:Energy Metabolism / Q000235:genetics; D005340:Fibrinogen / Q000235:genetics / Q000378:metabolism; D005432:Flounder / Q000235:genetics* / Q000378:metabolism; D005786:Gene Expression Regulation; D005880:Gills / Q000187:drug effects* / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007113:Immunity, Innate / Q000235:genetics; D058977:Molecular Sequence Annotation; D020543:Proteome / Q000235:genetics* / Q000378:metabolism; D013312:Stress, Physiological; D053719:Tandem Mass Spectrometry; D013696:Temperature
chemical_list: D051017:Apoptosis Regulatory Proteins; C115499:BBeta fibrinogen; D003176:Complement C3; D020543:Proteome; D002245:Carbon Dioxide; D005340:Fibrinogen