Temperature modulates the effects of ocean acidification on intestinal ion transport in Atlantic cod, Gadus morhua

CO₂-driven seawater acidification has been demonstrated to enhance intestinal bicarbonate secretion rates in teleosts, leading to an increased release of CaCO₃ under simulated ocean acidification scenarios. In this study, we investigated if increasing CO₂ levels stimulate the intestinal acid-base regulatory machinery of Atlantic cod (Gadus morhua) and whether temperatures at the upper limit of thermal tolerance stimulate or counteract ion regulatory capacities. Juvenile G. morhua were acclimated for 4 weeks to three CO₂ levels (550, 1200, and 2200 μatm) covering present and near-future natural variability, at optimum (10°C) and summer maximum temperature (18°C), respectively. Immunohistochemical analyses revealed the subcellular localization of ion transporters, including Na⁺/K⁺-ATPase (NKA), Na⁺/H⁺-exchanger 3 (NHE3), Na⁺/HCO3-cotransporter (NBC1), pendrin-like Cl-/HCO3-exchanger (SLC26a6), V-type H⁺-ATPase subunit a (VHA), and Cl- channel 3 (CLC3) in epithelial cells of the anterior intestine. At 10°C, proteins and mRNA were generally up-regulated for most transporters in the intestinal epithelium after acclimation to higher CO₂ levels. This supports recent findings demonstrating increased intestinal HCO3-secretion rates in response to CO₂ induced seawater acidification. At 18°C, mRNA expression and protein concentrations of most ion transporters remained unchanged or were even decreased, suggesting thermal compensation. This response may be energetically favorable to retain blood HCO3-levels to stabilize pH_e, but may negatively affect intestinal salt and water resorption of marine teleosts in future oceans.