Impacts of ocean acidification on respiratory gas exchange and acid–base balance in a marine teleost, Opsanus beta

Abstract

The oceanic carbonate system is changing rapidly due to rising atmospheric CO(2), with current levels expected to rise to between 750 and 1,000 μatm by 2100, and over 1,900 μatm by year 2300. The effects of elevated CO(2) on marine calcifying organisms have been extensively studied; however, effects of imminent CO(2) levels on teleost acid-base and respiratory physiology have yet to be examined. Examination of these physiological processes, using a paired experimental design, showed that 24 h exposure to 1,000 and 1,900 μatm CO(2) resulted in a characteristic compensated respiratory acidosis response in the gulf toadfish (Opsanus beta). Time course experiments showed the onset of acidosis occurred after 15 min of exposure to 1,900 and 1,000 μatm CO(2), with full compensation by 2 and 4 h, respectively. 1,900-μatm exposure also resulted in significantly increased intracellular white muscle pH after 24 h. No effect of 1,900 μatm was observed on branchial acid flux; however, exposure to hypercapnia and HCO(3)(-) free seawater compromised compensation. This suggests branchial HCO(3)(-) uptake rather than acid extrusion is part of the compensatory response to low-level hypercapnia. Exposure to 1,900 μatm resulted in downregulation in branchial carbonic anhydrase and slc4a2 expression, as well as decreased Na(+)/K(+) ATPase activity after 24 h of exposure. Infusion of bovine carbonic anhydrase had no effect on blood acid-base status during 1,900 μatm exposures, but eliminated the respiratory impacts of 1,000 μatm CO(2). The results of the current study clearly show that predicted near-future CO(2) levels impact respiratory gas transport and acid-base balance. While the full physiological impacts of increased blood HCO(3)(-) are not known, it seems likely that chronically elevated blood HCO(3)(-) levels could compromise several physiological systems and furthermore may explain recent reports of increased otolith growth during exposure to elevated CO(2).

Novel and potential physiological roles of vacuolar-type H+-ATPase in marine organisms

“…A few studies have reported downregulation of VHA mRNA in gills from fish exposed to OA (e.g. Esbaugh et al, 2012;Tseng et al, 2013), which, as pointed out in a recent review (Heuer and Grosell, 2014), was most likely due to downregulation of branchial HCO 3 − secretion to seawater and H + reabsorption into the blood.…”

Coral Reef Ecosystems under Climate Change and Ocean Acidification

“…At present, there are few reports on the influence or not of ocean acidification on the metabolic performance of tropical fish species. In this regard, it will be important to explore whether or not tropical fish have the same challenges that temperate fish have when it comes to respiratory gas transport and acid-base balance (Esbaugh et al, 2012;Pörtner et al, 2014). Physiological impacts combined with ecological impacts and habitat degradation, are likely to generate "surprises" for complex ecosystems such as those associated with both cold and warm water coral reefs.…”

Acid–base physiology, neurobiology and behaviour in relation to CO2-induced ocean acidification

“…P CO2 between 600 and 2000 µatm). The pattern that emerged was complete regulation of blood plasma pH and a 2-5 mmol l −1 increase in blood plasma [HCO 3 − ] Esbaugh et al, 2016Esbaugh et al, , 2012Green and Jutfelt, 2014;Heinrich et al, 2014;Heuer et al, 2016;Strobel et al, 2012) (Table 1). Only three studies measured blood plasma [Cl − ], but none of them found significant changes after exposure to OA-like conditions Green and Jutfelt, 2014;Heinrich et al, 2014).…”