Temperature Modulates the Effects of Ocean Acidification on Intestinal Ion Transport in Atlantic Cod, Gadus morhua

CO(2)-driven seawater acidification has been demonstrated to enhance intestinal bicarbonate secretion rates in teleosts, leading to an increased release of CaCO(3) under simulated ocean acidification scenarios. In this study, we investigated if increasing CO(2) 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 CO(2) 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(+)/ [Formula: see text] cotransporter (NBC1), pendrin-like Cl(−)/ [Formula: see text] 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 CO(2) levels. This supports recent findings demonstrating increased intestinal [Formula: see text] secretion rates in response to CO(2) 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 [Formula: see text] levels to stabilize pH(e,) but may negatively affect intestinal salt and water resorption of marine teleosts in future oceans.