Ocean Acidification Leads to Counterproductive Intestinal Base Loss in the Gulf Toadfish (Opsanus beta)

Oceanic CO2 has increased from 280 to 380 mu atm since pre-industrial times and is expected to reach 1,900 mu atm by 2300. In addition, regional upwelling zones exhibit levels up to 2,300 mu atm, making exploration at future global projected CO2 levels ecologically relevant today. Recent work has demonstrated that CO2 exposure as low as 1,000 mu atm induces acidosis in toadfish (Opansus beta), leading to metabolic compensation by retention of blood HCO3- in an effort to defend pH. Since increased serosal HCO3- translates to increased HCO3- secretion rates in isolated intestinal tissue, we predicted that blood elevation of HCO3- and Pco(2) during exposure to 1,900 mu atm CO2 would increase in vivo base secretion rates. Rectal fluid and CaCO3 excretions were collected from toadfish exposed to 380 (control) and 1,900 mu atm 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 mu atm CO2 exhibited higher rectal base excretion rates, higher rectal fluid HCO3- (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 intestinal loss, a process that acts against compensation for a CO2- HCO3- induced acidosis.