Acid-base balance compensation is the unifying course of CO2 impact in fish

Chair: Ivan Nagelkerken

Martin Grosell (1)*, Rachael Heuer (2)

1 RSMAS, University of Miami, Miami Florida, 33149 USA
2 Department of Biological Sciences, University of North Texas, Denton, Texas 76203 USA

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.

Gulf Toadfish (Opsanus beta) were exposed to CO2 ranging from background to 1900 µAtm. Intestinal tissue transport properties were analysed using in vitro techniques along with isolated tissue measurements in Ussing chambers. Furthermore, isolated tissue metabolic rate was assessed by respiromery.

The steady state of elevated pCO2 and [HCO3] seen during exposure to elevated CO2 appears to be the product of HCO3 uptake across the gill 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 results in a cascade of effects including altered intracellular acid-base balance and shifts in cellular transmembrane ion gradients with pronounced effects on sensory and central nervous system function.