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The Amazonian aquatic ecosystem undergoes seasonal variations and daily changes that directly affect the availability of oxygen. During the day the levels of oxygen can reach supersaturation, and at night can drop to zero. In this way, aquatic organisms are exposed daily to physiological challenges regarding the availability of oxygen. The present study revealed significant differences in the physiology and performance of two cichlids: Geophagus proximus (black water cichlid - from Negro River) and Chaetobranchopsis orbicularis (white water cichlid - from Amazon River), exposed to hypoxia. The white water cichlid showed lower value (1.99 ± 0.79 pKa) of critical pressure of oxygen (Pcrit) and a longer time (68.00 ± 14.11 min) for total loss of balance (LOE); however, this species showed 50% mortality during exposure to hypoxia, while the black water cichlid did not show mortality. Both cichlids presented a decrease in O 2 consumption rate (OCR) during hypoxia.. In this sense, it was observed that the black water cichlid presented several physiological strategies during hypoxia, such as, a significant increase in plasma cortisol levels, nucleoside triphosphate diphosphohydrolase activity (for adenosine diphosphate (ADP) as a substrate) in the gills, and the activity of adenosine deaminase (ADA) in gills and liver, in addition to a significant increase in the activity of complexes (II-III) in the transporter chain of electrons in both analyzed tissues and succinate dehydrogenase activity of gills' mitochondria. On the other hand, the only physiological change observed in the white water cichlid was a significant reduction in the activity of complexes II-III in gills and liver. Based on our findings, we can hypothesize that the white water cichlid specie has less tolerant to hypoxia when compared to the black water cichlid., (Copyright © 2021. Published by Elsevier Inc.)

The characteristics of the fish gill that maximize gas exchange are the same that promote diffusion of ions and water to and from the environment; therefore, physiological trade-offs are likely to occur. Here, we investigated how salinity acclimation affects whole-animal respiratory gas exchange during hypoxia using Fundulus heteroclitus , a fish that inhabits salt marshes where salinity and oxygen levels vary greatly. Salinity had marked effects on hypoxia tolerance, with fish acclimated to 11 and 35 ppt showing much longer time to loss of equilibrium (LOE) in hypoxia than 0 ppt-acclimated fish. Fish acclimated to 11 ppt (isosmotic salinity) exhibited the greatest capacity to regulate oxygen consumption rate ( Ṁ ) under hypoxia, as measured through the regulation index (RI) and O 2 ) under hypoxia, as measured through the regulation index (RI) and P crit extraction efficiency in normoxia and hypoxia, indicating a higher ventilatory workload in order to maintain similar levels of 2 These differences were related to alterations in gill morphology, where 0 ppt-acclimated fish had the smallest lamellar surface area with the greatest epithelial cell coverage (i.e. thicker lamellae, longer diffusion distance) and a larger interlamellar cell mass, contrasting with 11 ppt-acclimated fish, which had overall the highest respiratory surface area. The alteration of an array of physiological parameters provides evidence for a compromise between salinity and hypoxia tolerance in killifish acclimated to freshwater.2 extraction efficiency in normoxia and hypoxia, indicating a higher ventilatory workload in order to maintain similar levels of Ṁ O 2 These differences were related to alterations in gill morphology, where 0 ppt-acclimated fish had the smallest lamellar surface area with the greatest epithelial cell coverage (i.e. thicker lamellae, longer diffusion distance) and a larger interlamellar cell mass, contrasting with 11 ppt-acclimated fish, which had overall the highest respiratory surface area. The alteration of an array of physiological parameters provides evidence for a compromise between salinity and hypoxia tolerance in killifish acclimated to freshwater., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2019. Published by The Company of Biologists Ltd.)

We examined whether oxidative damage and antioxidant responses are more likely to occur during hypoxia or re-oxygenation in hypoxia-tolerant fish, and whether there is an influence of the rate of re-oxygenation. An hypoxia/re-oxygenation experiment using wild-caught Cyphocharax abramoides (Rio Negro, Brazil), was designed to answer these questions. Lipid peroxidation (MDA), a measure of oxidative damage, and antioxidant activities (superoxide dismutase (SOD), glutathione peroxidase (GPx), antioxidant capacity against peroxyl radicals (ACAP)), were measured in brain, gill and liver tissues after normoxia, 3-h hypoxia (2.7 kPa), and 3-h hypoxia followed by 1-h or 3-h re-oxygenation, implemented either immediately or slowly (3.0 kPa·h -1 ). Critical oxygen tension of routine oxygen consumption rate (Pcrit) (4.1 kPa) and the P O2 at loss of equilibrium (LOE) (1.7 kPa) were determined to set the experimental hypoxia exposure. The Regulation Index, a measure of oxyregulation with declining P O2 , was 0.32. Oxidative damage occurred during hypoxia: no additional damage was observed during re-oxygenation. Tissues responded differentially. GPx and MDA rose in the brain and gills, and SOD (and likely GPx) in the liver during hypoxia. Antioxidants increased further at LOE. Rate of oxygen increase during re-oxygenation did not affect antioxidant responses. In brain and gills, GPx and MDA decreased or recovered after 1-h re-oxygenation. In liver, SOD remained high and GPx increased. In summary, C. abramoides incurred oxidative damage during hypoxic exposure with no additional damage inflicted during re-oxygenation: the rate of re-oxygenation was inconsequential. Literature data support conclusion of greater damage during hypoxia than during re-oxygenation in hypoxia-tolerant fish., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Air breathing in fish is commonly believed to have arisen as an adaptation to aquatic hypoxia. The effectiveness of air breathing for tissue O 2 supply depends on the ability to avoid O 2 loss as oxygenated blood from the air-breathing organ passes through the gills. Here, we evaluated whether the armoured catfish (Hypostomus aff. pyreneusi)-a facultative air breather-can avoid branchial O 2 loss while air breathing in aquatic hypoxia, and we measured various other respiratory and metabolic traits important for O 2 supply and utilization. Fish were instrumented with opercular catheters to measure the O 2 tension (PO 2 ) of expired water, and air breathing and aquatic respiration were measured during progressive stepwise hypoxia in the water. Armoured catfish exhibited relatively low rates of O 2 consumption and gill ventilation, and gill ventilation increased in hypoxia due primarily to increases in ventilatory stroke volume. Armoured catfish began air breathing at a water PO 2 of 2.5 kPa, and both air-breathing frequency and hypoxia tolerance (as reflected by PO 2 at loss of equilibrium, LOE) was greater in individuals with a larger body mass. Branchial O 2 loss, as reflected by higher PO 2 in expired than in inspired water, was observed in a minority (4/11) of individuals as water PO 2 approached that at LOE. Armoured catfish also exhibited a gill morphology characterized by short filaments bearing short fused lamellae, large interlamellar cell masses, low surface area, and a thick epithelium that increased water-to-blood diffusion distance. Armoured catfish had a relatively low blood-O 2 binding affinity when sampled in normoxia (P 50 of 3.1 kPa at pH 7.4), but were able to rapidly increase binding affinity during progressive hypoxia exposure (to a P 50 of 1.8 kPa). Armoured catfish also had low activities of several metabolic enzymes in white muscle, liver, and brain. Therefore, low rates of metabolism and gill ventilation, and a reduction in branchial gas-exchange capacity, may help minimize branchial O 2 loss in armoured catfish while air breathing in aquatic hypoxia.

The primary goal of this study was to understand how changes in temperature and oxygen could influence social behaviour and aerobic metabolism of the Amazonian dwarf cichlid Apistogramma agassizii. Social hierarchies were established over a period of 96h by observing the social interactions, feeding behaviour and shelter use in groups of four males. In the experimental environment, temperature was increased to 29°C in the high-temperature treatment, and oxygen lowered to 1.0mg·L(-1)O2 in the hypoxia treatment. Fish were maintained at this condition for 96h. The control was maintained at 26°C and 6.6mg·L(-1)O2. After the experimental exposure, metabolism was measured as routine metabolic rate (RMR) and electron transport system (ETS) activity. There was a reduction in hierarchy stability at high-temperature. Aggression changed after environmental changes. Dominant and subdominant fish at high temperatures increased their biting, compared with control-dominant. In contrast, hypoxia-dominant fish decreased their aggressive acts compared with all other fish. Shelter use decreased in control and hypoxic dominant fish. Dominant fish from undisturbed environments eat more than their subordinates. There was a decrease of RMR in fish exposed to the hypoxic environment when compared with control or high-temperature fish, independent of social position. Control-dominant fish had higher RMR than their subordinates. ETS activity increased in fish exposed to high temperatures; however, there was no effect on social rank. Our study reinforces the importance of environmental changes for the maintenance of hierarchies and their characteristics and highlights that most of the changes occur in the dominant position., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Prochilodus nigricans, locally known as curimatã, is an Amazonian commercial fish that endures adverse environmental conditions, in particular low dissolved oxygen, during its migration. Poorer environmental conditions are expected in the near future. Prochilodus nigricans overcomes current seasonal and diurnal changes in dissolved oxygen by adjusting erythrocytic levels of ATP and GTP, modulators of Hb-O2 affinity. Will this fish species be endangered under more extreme environmental conditions as hypoxia and acidification tend to occur in a shorter period of time? As P. nigricans does not exhibit any apparent morphological alterations to exploit the air-water interface, it must rely on fast adjustments of blood properties. To investigate this aspect, basic hematology indices, pHe, pHi, plasma lactate, erythrocytic levels of ATP and GTP and functional properties of the hemolysate of P. nigricans were analyzed over a period of 6h in hypoxia and subsequent recovery in normoxia. The levels of erythrocytic GTP were four times higher than ATP and were reduced to ¼ of the original level after 3h under hypoxia. Erythrocytic levels of ATP were unaffected over the experimental period. All other analyzed blood parameters exhibited a time-course change in animals under hypoxia and returned to normoxic levels. Considering the hemolysate functional properties and the ability to regulate the above mentioned blood characteristics, P. nigricans is able to endure short-term changes in dissolved oxygen., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Oscars are often subjected to a combination of low levels of oxygen and fasting during nest-guarding on Amazonian floodplains. We questioned whether this anorexia would aggravate the osmo-respiratory compromise. We compared fed and fasted oscars (10-14 days) in both normoxia and hypoxia (10-20 Torr, 4 h). Routine oxygen consumption rates (O2) were increased by 75% in fasted fish, reflecting behavioural differences, whereas fasting improved hypoxia resistance and critical oxygen tensions (Pcrit) lowered from 54 Torr in fed fish to 34 Torr when fasting. In fed fish, hypoxia reduced liver lipid stores by approximately 50% and total liver energy content by 30%. Fasted fish had a 50% lower hepatosomatic index, resulting in lower total liver protein, glycogen and lipid energy stores under normoxia. Compared with hypoxic fed fish, hypoxic fasted fish only showed reduced liver protein levels and even gained glycogen (+50%) on a per gram basis. This confirms the hypothesis that hypoxia-tolerant fish protect their glycogen stores as much as possible as a safeguard for more prolonged hypoxic events. In general, fasted fish showed lower hydroxyacylCoA dehydrogenase activities compared with fed fish, although this effect was only significant in hypoxic fasted fish. Energy stores and activities of enzymes related to energy metabolism in muscle or gills were not affected. Branchial Na(+) uptake rates were more than two times lower in fed fish, whereas Na(+) efflux was similar. Fed and fasted fish quickly reduced Na(+) uptake and efflux during hypoxia, with fasting fish responding more rapidly. Ammonia excretion and K(+) efflux were reduced under hypoxia, indicating decreased transcellular permeability. Fasted fish had more mitochondria-rich cells (MRC), with larger crypts, indicating the increased importance of the branchial uptake route when feeding is limited. Gill MRC density and surface area were greatly reduced under hypoxia, possibly to reduce ion uptake and efflux rates. Density of mucous cells of normoxic fasted fish was approximately fourfold of that in fed fish. Overall, a 10-14 day fasting period had no negative effects on hypoxia tolerance in oscars, as fasted fish were able to respond more quickly to lower oxygen levels, and reduced branchial permeability effectively.

The aim of this study was to describe the effect of hypoxia on whole body ion fluxes and hematological parameters in two Amazonian teleosts: Serrasalmus eigenmanni and Metynnis hypsauchen. The increase of Na+ and Cl- effluxes on M. hypsauchen exposed to hypoxia may be related to an increase of gill ventilation and effective respiratory surface area, to avoid a reduction in the oxygen uptake, and/or with the decrease of pHe, that could inhibit Na+ and Cl- transporters and, therefore, reduce influx of these ions. Effluxes of Na+ and Cl- were lower in hypoxia than in normoxia for S. eigenmanni, possibly because in hypoxia this species would reduce gill ventilation and oxygen uptake, which would lead to a decrease of gill ion efflux and, consequently, reducing ion loss. The increase on hematocrit (Ht) during hypoxia in M. hypsauchen probably was caused by an increase of the red blood cell volume (MCV). For S. eigenmanni the increase on glucose possibly results from the usage of glucose reserve mobilization. Metynnis hypsauchen showed to be more sensitive to hypoxia than Serrasalmus eigenmanni, since the first presented more significant alterations on these osmoregulatory and hematological parameters. Nevertheless, the alterations observed for both species are strategies adopted by fishes to preserve oxygen supply to metabolizing tissues during exposure to hypoxia.

This study determined the respiratory responses to progressive hypoxia in oscar, an extremely hypoxia-tolerant Amazonian cichlid. Oscar depressed oxygen consumption rates (MO2), beginning at a critical O2 tension (Pcrit) of 46Torr, to only 14% of normoxic rates at 10Torr. Total ventilation (Vw) increased up to 4-fold, entirely due to a rise in ventilatory stroke volume (no change in ventilatory frequency), and water convection requirement (Vw/MO2) increased substantially (up to 15-fold). Gill O2 extraction fell steadily, from 60% down to 40%. Although O2 transfer factor (an index of gill O2 diffusion capacity) increased transiently in moderate hypoxia, it decreased at 10Torr, which may have caused the increased expired-arterial PO2 difference. Venous PO2 was always very low (< or =7Torr). Anaerobic metabolism made a significant contribution to ATP supply, indicated by a 3-fold increase in plasma lactate that resulted in an uncompensated metabolic acidosis. Respiration of isolated gill cells was not inhibited until below 5Torr; because gill water PO2 always exceeded this value, hypoxic ion flux arrest in oscars [Wood et al., Am. J. Physiol. Reg. Integr. Comp. Physiol. 292, R2048-R2058, 2007] is probably not caused by O2 limitation in ionocytes. We conclude that metabolic depression and tolerance of anaerobic bi-products, rather than a superior capacity for O2 supply, allow oscar to thrive in extreme hypoxia in the Amazon.

We examined the metabolic and ionoregulatory responses of the Amazonian cichlid, Astronotus ocellatus, to 20 h exposure to severe hypoxia (0.37 +/- 0.19 mg O(2)/l; 4.6% air saturation) or 8 h severe hypoxia followed by 12 h recovery in normoxic water. During 20 h exposure to hypoxia, white muscle [ATP] was maintained at normoxic levels primarily through a 20% decrease in [creatine phosphate] (CrP) and an activation of glycolysis yielding lactate accumulation. Muscle lactate accumulation maintained cytoplasmic redox state ([NAD(+)]/[NADH]) and was associated with an inactivation of the mitochondrial enzyme pyruvate dehydrogenase (PDH). The inactivation of PDH was not associated with significant changes in cytoplasmic allosteric modulators ([ADP(free)], redox state, or [pyruvate]). Hypoxia exposure caused an approximately 65% decrease in gill Na(+)/K(+) ATPase activity, which was not matched by changes in Na(+)/K(+) ATPase alpha-subunit protein abundance indicating post-translational modification of Na(+)/K(+) ATPase was responsible for the decrease in activity. Despite decreases in gill Na(+)/K(+) ATPase activity, plasma [Na(+)] increased, but this increase was possibly due to a significant hemoconcentration and fluid shift out of the extracellular space. Hypoxia caused an increase in Na(+)/K(+) ATPase alpha-subunit mRNA abundance pointing to either reduced mRNA degradation during exposure to hypoxia or enhanced expression of Na(+)/K(+) ATPase alpha-subunit relative to other genes.

The effects of graded hypoxia on the physiological and biochemical responses were examined in two closely related species of cichlids of the Amazon: Astronotus crassipinnis and Symphysodon aequifasciatus. Ten fish of each species were exposed to graded hypoxia for 8 h in seven oxygen concentrations (5.92, 3.15, 1.54, 0.79, 0.60, 0.34, and 0.06 mg O(2) L(-)(1)), with the aim to evaluate hypoxia tolerance and metabolic adjustments, where plasma glucose and lactate levels, hepatic and muscle glycogen contents, and maximum enzyme activities (PK, LDH, MDH and CS) in skeletal and cardiac muscles were measured. Another experimental set was done to quantify oxygen consumption (MO(2)) and opercular movements in two oxygen concentrations. Hypoxia tolerance differed between the two species. Astronotus crassipinnis was able to tolerate anoxia for 178 min while S. aequifasciatus was able to withstand 222 min exposure in deep hypoxia (0.75 mg O(2) L(-)(1)). Suppressed MO(2) was observed during exposure to 0.34 (A. crassipinnis) and 0.79 mg O(2) L(-)(1) (S. aequifasciatus), while opercular movements increased in both species exposed to hypoxia. Higher levels of muscle and liver glycogen and larger hypoxia-induced increases in plasma glucose and lactate were observed in A. crassipinnis, which showed a higher degree of hypoxia tolerance. Changes in enzyme levels were tissue-specific and differed between species suggesting differential abilities in down-regulating oxidative pathways and increasing anaerobic metabolism. Based on the present data, we conclude that these animals are good anaerobes and highly adapted to their environment, which is allowed by their abilities to regulate metabolic pathways and adjust their enzyme levels.

The contribution of alterations in mitochondrial K(ATP) channel activity and the sarcoplasmic reticulum (SR) to anaerobic cardiac function in the anoxia tolerant armored catfish Liposarcus pardalis were assessed. K(ATP) channels contribute to hypoxic cardioprotection in mammals, but little is known of their action in more hypoxia tolerant animals. Anoxia resulted in a decrease in force in isometrically contracting ventricle strips to approximately 40% of the pre-anoxic level. This was maintained for at least 2 h. Upon reoxygenation, hearts recovered to the same level as control preparations. Treatment with 5-hydroxydecanoic acid (5HD), a specific mitochondrial K(ATP) blocker significantly increased force in preparations during anoxia and caused hypercontracture at reoxygenation. Ryanodine, a specific inhibitor of SR function, significantly increased force loss in ventricle preparations under anoxia. Results show that mitochondrial K(ATP) channel activity and SR function are important in anaerobic and post-anaerobic contractility in armored catfish heart.

A wide range of organismic, physiological and biochemical adjustments to improve oxygen transfer is observed in fish exposed to environmental hypoxia and during anemia. Many fish species of the Amazon obtain oxygen directly from air when water oxygen is low. The accessory air-breathing organs include modifications of the gills, mouth, stomach and intestine, and swimbladder vascularization. Other species extend the lower lip and skim to improve oxygen uptake from the oxygen-rich surface layer of the water. The amount of oxygen uptake from air was estimated for Hoplosternum littorale and Lipossarcus pardalis. In addition, the oxygen uptake from the water surface was estimated for Colossoma macropomum. Blood oxygen content was reduced by 30% in Hoplosternum littorale and Colossoma macropomum and 70% in Lipossarcus pardalis if they were denied access to air. Adjustments of intraerythrocytic levels of ATP and GTP significantly improve oxygen transfer in fish during environmental hypoxia and anemia. In contrast to environmental hypoxia, intraerythrocytic levels of ATP and GTP increase during anemia in fish facilitating oxygen unloading to the tissues. It is suggested that the increase in ATP and GTP levels during anemia occurs because the conditions required to increase the activity of adenylate and guanylate phosphate synthetic pathways are similar.

The isozyme distribution of cichlid lactate dehydrogenase (LDH) is related to species environmental preferences. Cichlasoma amazonarum occurs in different environments and presents LDH tissue distribution patterns that correlate with oxygen tension at the capture location. Cichlasoma amazonarum was exposed to long-term severe hypoxia (51 days at 36.4 +/- 5.9 mmHg), tissue LDH isozyme distribution was analyzed by electrophoresis and enzyme activities were measured by monitoring the oxidation of NADH as pyruvate was reduced to lactate. The exposure of Cichlasoma amazonarum to long-term severe hypoxia resulted in changes in the tissue distribution of LDH isozymes. The major changes in response to hypoxia occurred in heart, liver and brain: isozyme A4 was activated in heart and brain, whereas isozyme B4 was activated in liver. The most significant quantitative change occurred in brain LDH of hypoxia-exposed animals which adopted muscle type kinetics, reflecting a new LDH isozyme distribution. LDH activity was significantly reduced (P < 0.05) in animals exposed to hypoxia (N = 8), suggesting an overall LDH suppression. Pyruvate inhibition decreased in all hypoxia-exposed tissues. Thus, the ability of Cichlasoma amazonarum to regulate LDH tissue expression according to oxygen availability allows the animal to survive chronic hypoxic environments. This phenotypic plasticity may occur in other hypoxia-tolerant fish species.