Schematic description of proposed processes in the gill epithelium of Hyas araneus in response intermediate P CO
exposure. Medium-term hypercapnia acclimation leads to a shift to a new acid–base equilibrium by accumulation of hemolymph bicarbonate (HCO3−). CO2 is hydrated into H+ and HCO3− by cytoplasmic carbonic anhydrase (CA). Protons are actively pumped out of the epithelial cell by an apical vacuolar proton ATPase (V(H+)-ATPase), followed by a transport of HCO3− via a basolateral anion exchanger (AE) and/or ion channel, such as bestrophin (Best1). Increased energy demand is in part met by an enhanced expression of complex I (CI) and complex IV (CIV) of the electron transport system and possibly triggered by a soluble adenylyl cyclase (sAC) induced signalling pathway. sAC is stimulated by HCO3− and increases the formation of cyclic adenosine monophosphate (cAMP), which activates protein kinase A (PKA) that subsequently leads to an induced expression of CI and CIV. While enhanced aerobic metabolic processes increase the generation of oxidants, the cellular defence against oxidative stress is adversely affected by a lower production of NADPH due to a decrease of the pentose phosphate pathway enzyme glucose-6-phosphate dehydrogenase (G6PD). NADPH acts as reducing agent for the regeneration of reduced glutathione (GSH) to oxidised glutathione (GSSH). The symbols (+) and (−) mark significantly up- and down-regulated genes, respectively modified after [55, 64].