Ocean acidification leads to counterproductive intestinal base loss in the gulf toadfish (Opsanus beta)

Oceanic CO₂ has increased from 280 to 380 μatm since preindustrial times and is expected to reach 1,900 μatm by 2300. In addition, regional upwelling zones exhibit levels up to 2,300 matm, making exploration at future global projected CO₂ levels ecologically relevant today. Recent work has demonstrated that CO₂ exposure as low as 1,000 μatm induces acidosis in toadfish (Opansus beta), leading to metabolic compensation by retention of blood in an effort to defend pH. Since increaseHCO^-₃ serosal HCO^-₃ translates to increased HCO^-₃ secretion rates in isolated intestinal tissue, we predicted that blood elevation of and Pco₂uring exposure to 1,900 μatm CO₂ HCO^-₃ would increase in vivo base secretion rates. Rectal fluid and CaCO₃ excretions were collected from toadfish exposed to 380 (control) and 1,900 μatm CO₂ for 72 h. Fluids were analyzed for pH, osmolality, ionic composition, and total CO₂. Precipitated CaCO₃ was analyzed for titratable alkalinity, Mg²⁺, and Ca²⁺ content. Fish exposed to 1,900 μatm CO₂ exhibited higher rectal base excretion rates, higher rectal fluid HCO^-₃ (mmol L^-1), and lower fluid Cl^- (mmol L^-1) than controls, suggesting increased intestinal anion exchange as a result of the compensated respiratory acidosis. This study verifies that imminent projected CO₂ levels expected by the year 2300 lead to greater HCO^-₃ intestinal loss, a process that acts against compensation for a CO_2- induced acidosis.