Acid-Base Balance Compensation Is the Unifying Cause of CO2 Impact in Fish

Fish are known to be excellent acid-base balance regulators and, by accumulation of plasma HCO₃^-, successfully defend blood pH at ambient partial pressures of CO₂ (pCO₂) as high as 50,000 µAtm. The reaction to elevated PCO₂ occurs within hours and persists for at least weeks leading to a new steady state of normalized pH but elevated plasma pCO₂ and [HCO₃^-] at levels as low as 750 µAtm. This steady state of elevated pCO₂ and [HCO₃^-] appears to be the product of HCO₃^- uptake rather than H⁺ extrusion and likely accounts for a number of observations of sublethal effects in fish exposed to environmentally relevant pCO₂ levels. Such observations include altered otolith growth presumably due to altered levels of substrate for CaCO₃ formation as well as altered transport of ion and acid-base equivalents by the marine fish intestinal epithelium and by the gill epithelium. The altered ion transport by osmoregulatory tissues has implications for integrative salt and water balance as well as energy utilization and consumption by these tissues. The protection of extracellular pH during CO₂ exposure is associated with altered intracellular acid-base balance and shifts in cellular transmembrane ion gradients. MG and RH are supported by the National Science Foundation.