Carbon dioxide induced plasticity of branchial acid-base pathways in an estuarine teleost

Anthropogenic CO2 is expected to drive ocean pCO(2) above 1,000 mu atm by 2100 - inducing respiratory acidosis in fish that must be corrected through branchial ion transport. This study examined the time course and plasticity of branchial metabolic compensation in response to varying levels of CO2 in an estuarine fish, the red drum, which regularly encounters elevated CO2 and may therefore have intrinsic resilience. Under control conditions fish exhibited net base excretion; however, CO2 exposure resulted in a dose dependent increase in acid excretion during the initial 2h. This returned to baseline levels during the second 2 h interval for exposures up to 5,000 mu atm, but remained elevated for exposures above 15,000 mu atm. Plasticity was assessed via gene expression in three CO2 treatments: environmentally realistic 1,000 and 6,000 mu atm exposures, and a proof-of-principle 30,000 ae atm exposure. Few differences were observed at 1,000 or 6,000 mu atm; however, 30,000 mu atm stimulated widespread up-regulation. Translocation of V-type ATPase after 1 h of exposure to 30,000 mu atm was also assessed; however, no evidence of translocation was found. These results indicate that red drum can quickly compensate to environmentally relevant acid-base disturbances using baseline cellular machinery, yet are capable of plasticity in response to extreme acid-base challenges.