Resilience to an acid-base disturbance and the development and plasticity of acid-base regulatory pathways in estuarine teleosts

Since the industrial revolution marine environments have displayed marked increases in CO₂ levels. Changes in ocean chemistry – collectively termed ocean acidification (OA) – are predicted to have numerous effects on marine fish, including critical behavioral endpoints and survival, with the most severe impacts hypothesized to occur in the vulnerable early life stages. However, many regions around the globe routinely have CO₂ levels in excess of those predicted by climate change, including the estuaries in the Gulf of Mexico, which are essential habitat for many ecologically and commercially important fish species. We hypothesize that the species that inhabit these environments contain physiological traits that confer resilience to OA. Thus, it is imperative that we understand the resilience of these species as well as the underlying mechanisms that may inform on the adaptive capacity of fish in general. The underlying physiological cause for many of the outcomes of OA is a systemic acid-base disturbance, which causes an elevated arterial pCO₂ and plasma [HCO₃⁻]. Because embryos and early life stage fish lack gills and practice cutaneous gas exchange, acid-base disturbances could be exacerbated in these life stages. Furthermore, little is known about the ontogeny, development, plasticity of acid-base regulatory mechanisms in early life stage marine fish, raising many questions about their ability to compensate for disturbance. Here we present work that shows tolerance of early life stage estuarine species to elevated CO₂ levels, including survival, standard length, and yolk size. However, we did observe significant heart rates in both studied estuarine species, and although we saw no immediate impacts, the long-term impacts of elevated heart rate are of keen interest. We also observed that alterations in acid-base regulatory machinery were the largely the result of development, rather than in response to exposure to an acid-base disturbance, including an acidosis and alkalosis. Although we did observe significant increases in NHE2 and VHA as the result of exposure to elevated CO₂ levels. Of interest is that H⁺ excretion was significant elevated in response to exposure to hypercapnia, and we hypothesize that this H⁺ excretion is the result of both the NHE and VHA pathway, from data obtained via the scanning ion-selective electrode technique (SIET) and pharmacological inhibition, but this must be further investigated