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

Abstract

Anthropogenic CO2 is expected to drive ocean pCO2 above 1,000 μatm 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 2 h. This returned to baseline levels during the second 2 h interval for exposures up to 5,000 μatm, but remained elevated for exposures above 15,000 μatm. Plasticity was assessed via gene expression in three CO2 treatments: environmentally realistic 1,000 and 6,000 μatm exposures, and a proof-of-principle 30,000 μatm exposure. Few differences were observed at 1,000 or 6,000 μatm; however, 30,000 μatm stimulated widespread up-regulation. Translocation of V-type ATPase after 1 h of exposure to 30,000 μatm 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.

Ocean acidification promotes broad transcriptomic responses in marine metazoans: a literature survey

“…Follow-up studies suggest that rather than a decreased production of ATP in response to OA, S. purpuatus larvae reallocate the total ATP produced; more ATP goes toward protein synthesis and ion transport when exposed to high pCO 2 , leaving less energy to maintain other cellular functions [83]. However, larvae from Strongylocentrotus purpuratus Embryos/Larvae [78][79][80][81][82][83][84][85][86] Adults [87] Chordata Fish Acanthochromis polyacanthus Juveniles [88,89] Dicentrarchus labrax Larvae [90] Gadus morhua Adults [91,92] Oryzias latipes Embryos/Hatchlings/Adults [93] Pagothenia borchgrevinki Adults [94] Sciaenops ocellatus Adults [95] Sebastes caurinus Juveniles [96] Sebastes mystinus Juveniles [96] Trematomus bernacchii Adults [97] Fig. 2 Exposure times in studies examining gene expression responses to ocean acidification across life-history stages.…”

Effects of Water Acidification on Senegalese Sole Solea senegalensis Health Status and Metabolic Rate: Implications for Immune Responses and Energy Use

“…This could impact fish acid-base balance, which results in the activation of regulatory mechanisms to compensate for the acidosis (Melzner et al, 2009) and initiates reflexes such as bradycardia and hyperventilation (Perry and Abdallah, 2012). Perry and Abdallah (2012) reviewed that changes in water CO 2 can be sensed by chemoreceptors mainly located in fish gills that are involved in elevating plasma HCO 3 − concentrations to compensate for the respiratory acidosis (Heuer and Grosell, 2014;Allmon and Esbaugh, 2017;Esbaugh, 2018). The marked effects of modest elevations in CO 2 in fish are due in part to the low physiological pCO 2 levels found in fish (Qin et al, 2010;Clements and Chopin, 2017).…”

Experimental Studies on the Impact of the Projected Ocean Acidification on Fish Survival, Health, Growth, and Meat Quality; Black Sea Bream (Acanthopagrus schlegelii), Physiological and Histological Studies

“…This inefficiency of the acid–base regulation is due to the long-term exposure to the acidic environment. [ 70 ] demonstrated earlier that a value of pCO 2 = 1000 µatm could lead to metabolic acidosis. Since the present study recorded a high pCO 2 value of 1993.71 ± 102.12 µatm in Predict_B, metabolic acidosis was expected.…”