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[Extract:] In their study, Clark et al. suggest that previous studies on the effects of elevated levels of CO2 on the behaviour of coral reef fishes are not repeatable and that ocean acidification does not impair the behaviour of coral reef fishes, even though six significant behavioural effects were detected in their study, each of which was dismissed for a different reason. They then compare the means and variances of six previous ocean acidification studies in fish with a data distribution that is derived from a multi-species compilation of their own data to conclude that the results of previous studies are statistically improbable. However, Clark et al. did not closely repeat previous studies, as they did not replicate key species, used different life stages and ecological histories and changed methods in important ways that reduce the likelihood of detecting the effects of ocean acidification.

Increases in ambient salinity demand parallel increases in intestinal base secretion for maintenance of osmoregulatory status, which is likely the cause of a transient acidosis following transfer of euryhaline fish from freshwater to seawater. It was predicted that transfer of the marine Gulf toadfish (Opsanus beta) from seawater (35 ppt) to hypersaline (60 ppt) seawater (HSW) would lead to a transient acidosis that would be compensated by increases in branchial acid excretion to offset the acid–base disturbance. Toadfish exposed to HSW showed a significant decrease in blood pH and [HCO3−] but no increase in pCO2, followed by a full recovery after 48–96 h. A similar metabolic acidosis and recovery was found when fish were exposed to 60-ppt HCO3−-free seawater (HEPES-buffered), which may suggest that compensation for intestinal base loss during hypersaline treatment is from gill H+ excretion rather than gill HCO3− uptake. However, we cannot rule out that reduced branchial HCO3− excretion contributed to an increase in net acid excretion. Since colchicine prevents full compensation, translocation of H+ and/or HCO3− transporters between cytosolic compartments and plasma membrane fractions might be involved in compensating for the hypersalinity-induced acidosis. Translocation of transporters rather than de novo synthesis may represent a faster and less energetically demanding response to rapidly fluctuating and high salinities encountered by toadfish in their natural environment.

Publicly available toxicological studies on wastewaters associated with unconventional oil and gas (UOG) activities in offshore regions are nonexistent. The current study investigated the impact of hydraulic fracturing-generated flowback water (HF-FW) on whole organism swimming performance/respiration and cardiomyocyte contractility dynamics in mahi-mahi (Coryphaena hippurus-hereafter referred to as "mahi"), an organism which inhabits marine ecosystems where offshore hydraulic fracturing activity is intensifying. Following exposure to 2.75% HF-FW for 24 h, mahi displayed significantly reduced critical swimming speeds (Ucrit) and aerobic scopes (reductions of ∼40 and 61%, respectively) compared to control fish. Additionally, cardiomyocyte exposures to the same HF-FW sample at 2% dilutions reduced a multitude of mahi sarcomere contraction properties at various stimulation frequencies compared to all other treatment groups, including an approximate 40% decrease in sarcomere contraction size and a nearly 50% reduction in sarcomere relaxation velocity compared to controls. An approximate 8-fold change in expression of the cardiac contractile regulatory gene cmlc2 was also seen in ventricles from 2.75% HF-FW-exposed mahi. These results collectively identify cardiac function as a target for HF-FW toxicity and provide some of the first published data on UOG toxicity in a marine species.

Deepwater Horizon crude oil is comprised of polycyclic aromatic hydrocarbons that cause a number of cardiotoxic effects in marine fishes across all levels of biological organization and at different life stages. Although cardiotoxic impacts have been widely reported, the mechanisms underlying these impairments in adult fish remain understudied. In this study, we examined the impacts of crude oil on cardiomyocyte contractility and electrophysiological parameters in freshly isolated ventricular cardiomyocytes from adult mahi-mahi (Coryphaena hippurus). Cardiomyocytes directly exposed to oil exhibited reduced contractility over a range of environmentally relevant concentrations (2.8-12.9 μg l-1∑PAH). This reduction in contractility was most pronounced at higher stimulation frequencies, corresponding to the upper limits of previously measured in situ mahi heart rates. To better understand the mechanisms underlying impaired contractile function, electrophysiological studies were performed, which revealed oil exposure prolonged cardiomyocyte action potentials and disrupted potassium cycling (9.9-30.4 μg l-1∑PAH). This study is the first to measure cellular contractility in oil-exposed cardiomyocytes from a pelagic fish. Results from this study contribute to previously observed impairments to heart function and whole-animal exercise performance in mahi, underscoring the advantages of using an integrative approach in examining mechanisms of oil-induced cardiotoxicity in marine fish.

Teleost fishes are diverse and successful, comprising almost half of all extant vertebrate species. It has been suggested that their success as a group is related, in part, to their unique O2 transport system, which includes pH-sensitive hemoglobin, a red blood cell β-adrenergic Na+/H+ exchanger (RBC β-NHE) that protects red blood cell pH, and plasma accessible carbonic anhydrase which is absent at the gills but present in some tissues, that short-circuits the β-NHE to enhance O2 unloading during periods of stress. However, direct support for this has only been examined in a few species of salmonids. Here, we expand the knowledge of this system to two warm-water, highly active marine percomorph fish, cobia (Rachycentron canadum) and mahi-mahi (Coryphaena hippurus). We show evidence for RBC β-NHE activity in both species, and characterize the Hb-O2 transport system in one of those species, cobia. We found significant RBC swelling following β-adrenergic stimulation in both species, providing evidence for the presence of a rapid, active RBC β-NHE in both cobia and mahi-mahi, with a time-course similar to that of salmonids. We generated oxygen equilibrium curves (OECs) for cobia blood and determined the P50, Hill, and Bohr coefficients, and used these data to model the potential for enhanced O2 unloading. We determined that there was potential for up to a 61% increase in O2 unloading associated with RBC β-NHE short-circuiting, assuming a - 0.2 ∆pHa-v in the blood. Thus, despite phylogenetic and life history differences between cobia and the salmonids, we found few differences between their Hb-O2 transport systems, suggesting conservation of this physiological trait across diverse teleost taxa.

Despite having an aglomerular kidney, Gulf toadfish can survive in water ranging from nearly fresh up to 70 parts per thousand salinity. In hyperosmotic environments, the major renal function is to balance the passive Mg2+ load from the environment with an equal excretion. However, the molecular transporters involved in Mg2+ secretion are poorly understood. We investigated whether environmental MgCl2 alone or in combination with elevated salinity affected transcriptional regulation of genes classically involved in renal Mg2+ secretion (slc41a1, slc41a3, cnnm3) together with three novel genes (trpm6, trpm7, claudin-19) and two isoforms of the Na+/K+-ATPase α-subunit (nka-α1a, nka-α1b). First, toadfish were acclimated to 5, 9, 35, or 60 ppt water (corresponding to ~ 7, 13, 50 and 108 mmol L−1 ambient [Mg2+], respectively) and sampled at 24 h or 9 days. Next, the impact of elevated ambient [Mg2+] was explored by exposing toadfish to control (50 mmol L−1 Mg2+), or elevated [Mg2+] (100 mmol L−1) at a constant salinity for 7 days. Mg2+ levels in this experiment corresponded with levels in control and hypersaline conditions in the first experiment. A salinity increase from 5 to 60 ppt stimulated the level of all investigated transcripts in the kidney. In Mg2+-exposed fish, we observed a 14-fold increase in the volume of intestinal fluids and elevated plasma osmolality and [Mg2+], suggesting osmoregulatory challenges. However, none of the renal gene targets changed expression compared with the control group. We conclude that transcriptional regulation of renal Mg2+ transporters is induced by elevated [Mg2+] in combination with salinity rather than elevated ambient [Mg2+] alone.

Pelagic fish embryos are thought to float in or near surface waters for the majority of their development and are presumed to have little to no control over their mobility, rendering these embryos at high risk for damages associated with surface stressors such as ultraviolet radiation (UVR). We recently challenged these long-standing paradigms by characterizing a potential mechanism of stressor avoidance in early-life stage mahi-mahi (Coryphaena hippurus) in which embryos sense external cues, such as UVR, and modify their buoyancy to reduce further exposure. It is unknown whether embryos of other marine fish with pelagic spawning strategies have similar capabilities. To fill this knowledge gap, we investigated buoyancy change in response to UVR in three additional species of marine fish that utilize a pelagic spawning strategy: yellowfin tuna (Thunnus albacares), red snapper (Lutjanus campechanus), and cobia (Rachycentron canadum). Embryos of all three species displayed increased specific gravity and loss of buoyancy after exposures to environmentally relevant doses of UVR, a response that may be ubiquitous to fish with pelagic embryos. To gain further insight into this response, we investigated recovery of buoyancy, oxygen consumption, energy depletion, and photolyase induction in response to UVR exposures in at least one of the three species listed above.

Mahi-mahi (Coryphaena hippurus) are a highly migratory pelagic fish, but little is known about what environmental factors drive their broad distribution. This study examined how temperature influences aerobic scope and swimming performance in mahi. Mahi were acclimated to four temperatures spanning their natural range (20, 24, 28, and 32{\deg}C; 5-27 days) and critical swimming speed (Ucrit), metabolic rates, aerobic scope, and optimal swim speed were measured. Aerobic scope and Ucrit were highest in 28{\deg}C-acclimated fish. 20{\deg}C-acclimated mahi experienced significantly decreased aerobic scope and Ucrit relative to 28{\deg}C-acclimated fish (57 and 28% declines, respectively). 32{\deg}C-acclimated mahi experienced increased mortality and a significant 23% decline in Ucrit, and a trend for a 26% decline in factorial aerobic scope relative to 28{\deg}C-acclimated fish. Absolute aerobic scope showed a similar pattern to factorial aerobic scope. Our results are generally in agreement with previously observed distribution patterns for wild fish. Although thermal performance can vary across life stages, the highest tested swim performance and aerobic scope found in the present study (28{\deg}C), aligns with recently observed habitat utilization patterns for wild mahi and could be relevant for climate change predictions., Comment: 24 pages, 3 figures main text, 6 figures supplemental text, published in Frontiers in Marine Science https://www.frontiersin.org/articles/10.3389/fmars.2021.654276/full

Despite having an aglomerular kidney, Gulf toadfish can survive in water ranging from nearly fresh up to 70 parts per thousand salinity. In hyperosmotic environments, the major renal function is to balance the passive Mg

Publicly available toxicological studies on wastewaters associated with unconventional oil and gas (UOG) activities in offshore regions are nonexistent. The current study investigated the impact of hydraulic fracturing-generated flowback water (HF-FW) on whole organism swimming performance/respiration and cardiomyocyte contractility dynamics in mahi-mahi (

Aerobic exercise capacity is dependent on the cardiorespiratory system's ability to supply oxygen at a rate that meets energetic demands. In teleost fish crude oil exposure, with the associated polycyclic aromatic hydrocarbons (PAH's), reduces exercise performance and this has been hypothesized to be due to compromised cardiovascular function. In this study, we test this hypothesis by simultaneously measuring cardiovascular performance, oxygen consumption, and swim performance in a pelagic teleost, the cobia (Rachycentron canadum). Metabolic rate increased over 300% in both groups during the swim trial but as the fish approached the critical swim speed (Ucrit) MO2 was 12% lower in the oil exposed fish. Further, stroke volume was initially 35% lower while heart rate was 15% higher in the oil exposed compared to control fish. Our findings suggested, while aspects of cardiovascular and metabolic function are altered by oil exposure, additional studies are needed to further understand the homeostatic mechanisms that may sustain cardiovascular function at higher exercise intensities in cobia.

Increases in ambient salinity demand parallel increases in intestinal base secretion for maintenance of osmoregulatory status, which is likely the cause of a transient acidosis following transfer of euryhaline fish from freshwater to seawater. It was predicted that transfer of the marine Gulf toadfish (Opsanus beta) from seawater (35 ppt) to hypersaline (60 ppt) seawater (HSW) would lead to a transient acidosis that would be compensated by increases in branchial acid excretion to offset the acid-base disturbance. Toadfish exposed to HSW showed a significant decrease in blood pH and [HCO

Estuarine crocodiles Crocodylus porosus inhabit freshwater, estuarine and marine environments. Despite being known to undertake extensive movements throughout and between hypo- and hyperosmotic environments, little is known on the role of the cloaca in coping with changes in salinity. In addition to the well-documented functional plasticity of the lingual salt glands, we report here that the middle of the three cloacal segments (i.e. the urodaeum), responds to increased ambient salinity to enhance solute-coupled water absorption. This post-renal modification of urine serves to conserve water when exposed to hyperosmotic environments and, in conjunction with lingual salt gland secretions, enables C. porosus to maintain salt and water balance and thereby thrive in hyperosmotic environments. Isolated epithelia from the urodaeum of 70% seawater-acclimated C. porosus had a strongly enhanced short circuit current (indicator of active ion transport) compared to freshwater-acclimated crocodiles. This enhanced active ion absorption was driven by increased Na+/K+-ATPase activity, and possibly enhanced proton pump activity, and was facilitated by the apical epithelial Na+ channel (ENaC) and/or the apical Na+/H+ exchanger (NHE2), both of which are expressed in the urodaeum. NHE3 was expressed at very low levels in the urodaeum and likely does not contribute to solute-coupled water absorption in this cloacal segment. Since C. porosus does not appear to drink water of salinities above 18 ppt, observations of elevated short circuit current in the rectum as well as a trend for increased NHE2 expression in the esophagus, the anterior intestine, and the rectum, suggests that dietary salt intake may stimulate salt, and possibly water absorption by the gastro-intestinal tract of C. porosus living in hyperosmotic environments.

An understudied consequence of coastal urbanization on marine environments is sound pollution. While underwater anthropogenic sounds are recognized as a threat to aquatic organisms, little is known about the effects of above-surface coastal sound pollution on adjacent underwater soundscapes and the organisms inhabiting them. Here, the impact of noise from the 2019 Ultra Music Festival® in Miami, FL, USA was assessed at the University of Miami Experimental Hatchery (UMEH) located directly adjacent to the music festival and on underwater sound levels in Bear Cut, a nearby water channel. In addition, stress hormone levels in fish held at UMEH were measured before and during the festival. Air sound levels recorded at UMEH during the Ultra Music Festival did not exceed 72 dBA and 98 dBC. The subsurface sound intensity levels in the low frequency band increased by 2–3 dB re 1 μPa in the adjacent waterway, Bear Cut, and by 7–9 dB re 1 μPa in the fish tanks at UMEH. Gulf toadfish (Opsanus beta) housed in the UMEH tanks experienced a 4–5 fold increase in plasma cortisol, their main stress hormone, during the first night of the Ultra Music Festival compared to two baseline samples taken 3 weeks and 4 days before Ultra. While this study offers preliminary insights into this type of sound pollution, more research is needed to conclude if Ultra caused a stress response in wild organisms and to fully understand the implications of this type of sound pollution.

Estuarine crocodiles

Exposure to polycyclic aromatic hydrocarbons (PAH) negatively impacts exercise performance in fish species but the physiological modifications that result in this phenotype are poorly understood. Prior studies have shown that embryonic and juvenile mahi–mahi (Coryphaeus hippurus) exposed to PAH exhibit morphological abnormalities, altered cardiac development and reduced swimming performance. It has been suggested that cardiovascular function inhibited by PAH exposure accounts for the compromised exercise performance in fish species. In this study we used in-situ techniques to measure hemodynamic responses of young adult mahi–mahi exposed to PAH for 24 h. The data indicate that stroke volume was reduced 44% in mahi–mahi exposed to 9.6 ± 2.7 μg l−1 geometric mean PAH (∑PAH) and resulted in a 39% reduction in cardiac output and a 52% reduction in stroke work. Maximal change in pressure over change in time was 28% lower in mahi–mahi exposed to this level of ∑PAH. Mean intraventricular pressures and heart rate were not significantly changed. This study suggests exposure to environmentally relevant PAH concentrations impairs aspects of cardiovascular function in mahi–mahi.

Most marine teleosts defend blood pH during high CO2 exposure by sustaining elevated levels of HCO3(-) in body fluids. In contrast to the gill, where measures are taken to achieve net base retention, elevated CO2 leads to base loss in the intestine of marine teleosts studied to date. This loss is thought to occur through transport pathways previously demonstrated to be involved with routine osmoregulation in marine teleosts. The main objective of this study was to characterize the intestinal transport physiology of the gulf toadfish (Opsanus beta) when exposed to varied levels of CO2: control, 5,000, 10,000, and 20,000 μatm CO2 (0.04, 0.5, 1, and 2 kPa, respectively). Results of this study suggest that intestinal apical anion exchange is highly responsive to hypercarbia, evidenced by a dose-dependent increase in intestinal luminal HCO3(-) (mmol L(-1)) that was mirrored by a reduction in Cl(-) (mmol L(-1)). Despite activation of HCO3(-) transport pathways typically used during osmoregulation, fractional fluid absorption was only significantly lower at the highest level of CO2. Although increased HCO3(-) excretion could provide more substrate for intestinally produced carbonates, carbonate production was not significantly increased during hypercarbia at the levels tested. This study is among the first to thoroughly characterize how compensation for elevated CO2 affects transport physiology and carbonate production in the marine fish intestine. This deeper understanding may be particularly relevant when considering the impacts of future predicted ocean acidification, where prolonged base loss may alter the energetic cost of acid-base balance or osmoregulation in marine fish.

Mitochondrial function is critical to support aerobic metabolism through the production of ATP, and deficiencies in mitochondrial bioenergetics will directly impact the performance capacity of highly aerobic tissues such as the myocardium. Cardiac function in fish has been shown to be negatively affected by crude oil exposure, however, the mechanism for this adverse response is largely unexplored. We hypothesized that lipophilic polycyclic aromatic hydrocarbons (PAHs) found in crude oil disrupt the electron transport system (ETS) ultimately leading to mitochondrial dysfunction. In this study, mitochondrial respiration and ADP affinity we measured using high resolution respirometery in permeabilized cardiac muscle fibers of young adult Mahi-mahi (Coryphaena hippurus) after an acute (24 h) whole animal crude oil exposure. Oil exposure reduced both complex I-fueled ADP stimulated respiration (OXPHOSCI) and complex I,II-fueled ADP stimulated respiration (OXPHOSCI, CII) by 33%,while complex II-fueled ADP stimulated respiration (OXPHOSCII) was reduced by 25%. These changes were found without changes in enzyme activity or mitochondrial density between control and oil exposed Mahi. Additionally, mitochondrial affinity for ADP was decreased three-fold after acute exposure to crude oil. We purpose that acute crude oil exposure selectively impairs mitochondrial complexes of the electron transport system and ATP supply to the cell. This limited ATP supply could present several challenges to a predatory animal like the mahi; including a reliance on anaerobic metabolism and ultimately cell or tissue death as metabolic substrates are rapidly depleted. However, the impact of this impairment may only be evident under periods of increased aerobic metabolic demand.

Recent experimental studies show that relatively small increases in environmental CO2 can fundamentally alter the behavior of marine and freshwater fishes by altering and/or impairing the function of neurotransmitter receptors. Most evidence to date suggests that the underlying mechanism of these behavioral disruptions is linked to alterations of ion gradients across the GABAA receptor, responsible for inhibitory input in neural circuits throughout the nervous system. This chapter will describe the mechanism(s) through which acid-base compensation during exposure to high CO2 has downstream neurophysiological effects in fish, including new molecular evidence for a self-amplifying cycle in GABAergic neurotransmission during high CO2 exposure.

Aqueous crude oil spills expose fish to varying concentrations of dissolved polycyclic aromatic hydrocarbons (PAHs), which can have lethal and sublethal effects. The heart is particularly vulnerable in early life stages, as PAH toxicity causes developmental cardiac abnormalities and impaired cardiovascular function. However, cardiac responses of juvenile and adult fish to acute oil exposure remain poorly understood. We sought to assess cardiac function in a pelagic fish species, the cobia (Rachycentron canadum), following acute (24 h) exposure to two ecologically relevant levels of dissolved PAHs. Cardiac power output (CPO) was used to quantify cardiovascular performance using an in situ heart preparation. Cardiovascular performance was varied using multiple concentrations of the β-adrenoceptor agonist isoproterenol (ISO) and by varying afterload pressures. Oil exposure adversely affected CPO with control fish achieving maximum CPO’s (4 mW g–1 Mv) greater than that of oil-exposed fish (1 mW g–1 Mv) at ISO...

Energetic costs associated with ion and acid-base regulation in response to ocean acidification have been predicted to decrease the energy available to fish for basic life processes. However, the low cost of ion regulation (6–15% of standard metabolic rate) and inherent variation associated with whole-animal metabolic rate measurements have made it difficult to consistently demonstrate such a cost. Here we aimed to gain resolution in assessing the energetic demand associated with acid-base regulation by examining ion movement and O2 consumption rates of isolated intestinal tissue from Gulf toadfish acclimated to control or 1900 μatm CO2 (projected for year 2300). The active marine fish intestine absorbs ions from ingested seawater in exchange for HCO3− to maintain water balance. We demonstrate that CO2 exposure causes a 13% increase of intestinal HCO3− secretion that the animal does not appear to regulate. Isolated tissue from CO2-exposed toadfish also exhibited an 8% higher O2 consumption rate than tissue from controls. These findings show that compensation for CO2 leads to a seemingly maladaptive persistent base (HCO3−) loss that incurs an energetic expense at the tissue level. Sustained increases to baseline metabolic rate could lead to energetic reallocations away from other life processes at the whole-animal level.

Neurosensory and behavioural disruptions are some of the most consistently reported responses upon exposure to ocean acidification-relevant CO2 levels, especially in coral reef fishes. The underlying cause of these disruptions is thought to be altered current across the GABAA receptor in neuronal cells due to changes in ion gradients (HCO3− and/or Cl−) that occur in the body following compensation for elevated ambient CO2. Despite these widely-documented behavioural disruptions, the present study is the first to pair a behavioural assay with measurements of relevant intracellular and extracellular acid-base parameters in a coral reef fish exposed to elevated CO2. Spiny damselfish (Acanthochromis polyacanthus) exposed to 1900 μatm CO2 for 4 days exhibited significantly increased intracellular and extracellular HCO3− concentrations and elevated brain pHi compared to control fish, providing evidence of CO2 compensation. As expected, high CO2 exposed damselfish spent significantly more time in a chemical alarm cue (CAC) than control fish, supporting a potential link between behavioural disruption and CO2 compensation. Using HCO3− measurements from the damselfish, the reversal potential for GABAA (EGABA) was calculated, illustrating that biophysical properties of the brain during CO2 compensation could change GABAA receptor function and account for the behavioural disturbances noted during exposure to elevated CO2.

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).

Most fish studied to date efficiently compensate for a hypercapnic acid-base disturbance; however, many recent studies examining the effects of ocean acidification on fish have documented impacts at CO2levels predicted to occur before the end of this century. Notable impacts on neurosensory and behavioral endpoints, otolith growth, mitochondrial function, and metabolic rate demonstrate an unexpected sensitivity to current-day and near-future CO2levels. Most explanations for these effects seem to center on increases in Pco2and HCO3−that occur in the body during pH compensation for acid-base balance; however, few studies have measured these parameters at environmentally relevant CO2levels or directly related them to reported negative endpoints. This compensatory response is well documented, but noted variation in dynamic regulation of acid-base transport pathways across species, exposure levels, and exposure duration suggests that multiple strategies may be utilized to cope with hypercapnia. Understanding this regulation and changes in ion gradients in extracellular and intracellular compartments during CO2exposure could provide a basis for predicting sensitivity and explaining interspecies variation. Based on analysis of the existing literature, the present review presents a clear message that ocean acidification may cause significant effects on fish across multiple physiological systems, suggesting that pH compensation does not necessarily confer tolerance as downstream consequences and tradeoffs occur. It remains difficult to assess if acclimation responses during abrupt CO2exposures will translate to fitness impacts over longer timescales. Nonetheless, identifying mechanisms and processes that may be subject to selective pressure could be one of many important components of assessing adaptive capacity.

Oceanic CO(2) has increased from 280 to 380 μatm since preindustrial times and is expected to reach 1,900 μatm by 2300. In addition, regional upwelling zones exhibit levels up to 2,300 μatm, making exploration at future global projected CO(2) levels ecologically relevant today. Recent work has demonstrated that CO(2) exposure as low as 1,000 μatm induces acidosis in toadfish (Opansus beta), leading to metabolic compensation by retention of blood HCO(3) in an effort to defend pH. Since increased serosal HCO(3) translates to increased HCO(3) rates in isolated intestinal tissue, we predicted that blood elevation of HCO(3) and Pco(2) during exposure to 1,900 μatm CO(2) would increase in vivo base secretion rates. Rectal fluid and CaCO(3) excretions were collected from toadfish exposed to 380 (control) and 1,900 μatm CO(2) for 72 h. Fluids were analyzed for pH, osmolality, ionic composition, and total CO(2). Precipitated CaCO(3) was analyzed for titratable alkalinity, Mg(2+), and Ca(2+) content. Fish exposed to 1,900 μatm CO(2) exhibited higher rectal base excretion rates, higher rectal fluid HCO(3) (mmol L(-1)), and lower fluid Cl(-) (mmol L(-1)) than controls, suggesting increased intestinal anion exchange as a result of the compensated respiratory acidosis. This study verifies that imminent projected CO(2) levels expected by the year 2300 lead to greater intestinal HCO(3) loss, a process that acts against compensation for a CO(2)-induced acidosis.