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

Oceanic CO(2) 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 μatm, making exploration at future global projected CO(2) levels ecologically relevant today. Recent work has demonstrated that CO(2) exposure as low as 1,000 μatm induces acidosis in toadfish (Opansus beta), leading to metabolic compensation by retention of blood HCO(3) in an effort to defend pH. Since increased serosal HCO(3) translates to increased HCO(3) rates in isolated intestinal tissue, we predicted that blood elevation of HCO(3) and Pco(2) during exposure to 1,900 μatm CO(2) would increase in vivo base secretion rates. Rectal fluid and CaCO(3) excretions were collected from toadfish exposed to 380 (control) and 1,900 μatm CO(2) for 72 h. Fluids were analyzed for pH, osmolality, ionic composition, and total CO(2). Precipitated CaCO(3) was analyzed for titratable alkalinity, Mg(2+), and Ca(2+) content. Fish exposed to 1,900 μatm CO(2) 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 CO(2) levels expected by the year 2300 lead to greater intestinal HCO(3) loss, a process that acts against compensation for a CO(2)-induced acidosis.