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The electrolytic manganese industry produces a large amount of electrolytic manganese residue (EMR). Soluble Mn, NH 4 +-N, and other pollutants may be released from the open-air stacked EMR and transported to the environment along with rainfall or surface runoff. Aqueous EMR solution (AES) generally contains various elements required for plant growth, and phytoremediation can be applied to remove these pollutants from AES. Since the contents of Fe and Co vary greatly in AES depending on the ore sources as well as the pre-treatment processes, the presence of bioavailable Fe and Co at different levels may affect plant growth, the rhizosphere microbes, and pollutant removal. The present study investigated the in-situ removal of Mn(II) and NH 4 +-N from AES solution using free floating aquatic plant Pistia stratiotes , focusing especially on the effects of Fe/Co presence and rhizospheric microbe synergistic involvement on contaminant removal. The results showed that 69.08% of Mn and 94.99% of NH 4 +-N were removed by P. stratiotes in 24 d. Both the presence of Fe(II) and Co(II) facilitated the Mn(II) immobilization and increased Mn(II) removal by 19–31% due to the enhanced peroxidase activity and the increased Mn accumulating in roots The complete removal of Mn from AES was found in the presence of Fe(II) at 2 mg L−1 or Co(II) at 0.5 mg L−1 and more than 51% accumulated Mn in the roots was stored in the vacuole and cytoplasm. BioMnO x was found on the surface of the roots, revealing that rhizofiltration, rhizospheric plaque/biofilm formation, and Mn biogeochemical cycle exert synergic effects on Mn(II) immobilization. The findings of the present study demonstrate the feasibility of using P. stratiotes in the treatment of aqueous EMR solutions and the presence of an appropriate amount of bio-available Fe and Co can promote the removal of Mn(II) and NH 4 +-N. [Display omitted] • Up to 100% of Mn can be removed from AES by P. stratiotes. • Co(II) and Fe(II) promoted the root secretion of tartaric and citric acids. • Microbial-involved Mn cycling accelerated the fixation of metals on root surface. • Both Fe and Co affected rhizosphere micro-eukaryotic community composition. • Fe and Mn transport function of EBs was more abundant with the presence of Fe/Co. [ABSTRACT FROM AUTHOR]

The Alaska blackfish (Dallia pectoralis) is the only air-breathing fish in the Arctic. In the summer, a modified esophagus allows the fish to extract oxygen from the air, but this behavior is not possible in the winter because of ice and snow cover. The lack of oxygen (hypoxia) and near freezing temperatures in winter is expected to severely compromise metabolism, and yet remarkably, overwintering Alaska blackfish remain active. To maintain energy balance in the brain and limit the accumulation of reactive oxygen species (ROS), we hypothesized that cold hypoxic conditions would trigger brain mitochondrial remodeling in the Alaska blackfish. To address this hypothesis, fish were acclimated to warm (15 °C) normoxia, cold (5 °C) normoxia or cold hypoxia (5 °C, 2.1–4.2 kPa; no air access) for 5–8 weeks. Mitochondrial respiration, ADP affinity and H 2 0 2 production were measured at 10 °C in isolated brain homogenates with an Oroboros respirometer. Cold acclimation and chronic hypoxia had no effects on mitochondrial aerobic capacity or ADP affinity. However, cold acclimation in normoxia led to a suppression of brain mitochondrial H 2 0 2 production, which persisted and became more pronounced in the cold hypoxic fish. Overall, our study suggests cold acclimation supresses ROS production in Alaska blackfish, which may protect the fish from oxidative stress when oxygen becomes limited during winter. [Display omitted] • Alaska blackfish overwinter under ice-covered lakes in severely hypoxic conditions • We hypothesized survival of these winter conditions would require metabolic readjustments • Cold acclimation and chronic hypoxia suppressed brain reactive oxygen species (ROS) production • Suppression of ROS production may protect the fish from oxidative stress during winter [ABSTRACT FROM AUTHOR]

Climate change and urbanisation of watercourses affect water temperatures and current flow velocities in river systems on a global scale. This represents a particularly critical issue for migratory fish species with complex life histories that use rivers to reproduce. Salmonids are migratory keystone species that provide substantial economical value to ecosystems and human societies. Consequently, a comprehensive understanding of the effects of environmental stressors on their reproductive success is critical in order to ensure their continued abundance during future climatic change. Salmonids are capital breeders, relying entirely on endogenous energy stores to fuel return migration to their natal spawning sites and reproduction upon arrival. Metabolic rates and cost of transport en-route increase with temperature and at extreme temperatures, swimming is increasingly fuelled anaerobically, resulting in an oxygen debt and reduced capacity to recover from exhaustive exercise. Thermally challenged salmonids also produce less viable gametes, which themselves are affected by water temperature after release. Passage through hydrological barriers and temperature changes both affect energy expenditure. As a result, important energetic tradeoffs emerge between extra energy used during migration and that available for other facets of the reproductive cycle, such as reproductive competition and gamete production. However, studies identifying these tradeoffs are extremely sparse. This review focuses on the specific locomotor responses of salmonids to thermal and hydrological challenges, identifying gaps in our knowledge and highlighting the potential implications for key aspects of their reproduction. [ABSTRACT FROM AUTHOR]

Abstract: Mammalian cardiac muscle exhibits a number of intrinsic response systems which adjust function to changing conditions. These include the Frank–Starling response and the slow force response which are activated upon myocardial stretch, and the force–frequency response, which is evident upon changes in cardiac frequency. In this study we have examined the effect of myocardial stretch and changes in pacing frequency on isolated ventricular muscle preparations from the ectothermic amphibian, the axolotl (Ambystoma mexicanum). We preformed these studies at two physiologically relevant temperatures 17°C and 21°C. We found that increasing the length of the muscle increased active force via the Frank–Starling response at both temperatures, which is consistent with cardiac muscle preparations in other vertebrates. We found no evidence for the slow force response at either temperature suggesting that in axolotl, unlike mammals but similar to fish, the slow force response is not associated with the Frank–Starling response. Increasing contraction frequency caused a decrease in active force across all frequencies tested (0.5−2.0Hz)—a monophasic negative force–frequency response, independent of temperature. [Copyright &y& Elsevier]

Ultrastructure, molecular composition and electrophysiological properties of cardiac myocytes and functional characteristics of the fish heart suggest that cycling of extracellular Ca2+ is generally more important than intracellular cycling of Ca2+ stores of the sarcoplasmic reticulum (SR) in activating contraction of fish cardiac myocytes. This is especially true for the ventricle. However, prominent species-specific differences exist in cardiac excitation-contraction coupling and in the relative roles of extracellular and intracellular Ca2+ sources among the teleostean fish. In fact, in some fish species (tunas, burbot) the SR of atrial myocytes, under certain circumstances, may act as the major source of systolic Ca2+. These interspecific differences are obviously an outcome of evolutionary adaptation to different habitats and modes of activity in these habitats. There is also substantial intraspecific variation in the SR Ca2+-release-to-SL-Ca2+ influx ratio depending on acute and chronic temperature changes. Consequently excitation-contraction coupling of the fish cardiac myocytes is not a fixed entity, but rather a highly variable and malleable process that enables fish to have an appropriate cardiac scope to exploit a diverse range of environments. [Copyright &y& Elsevier]

Exploitation of offshore oil reserves, heightened traffic in marine transportation routes, and the release of petrochemicals from the thawing of permafrost and glaciers is increasing the bioavailability of polycyclic aromatic hydrocarbons (PAHs) to aquatic organisms. This availability may also change with the seasons as temperature changes accessibility of Arctic transport routes and the degree of land- and ice-melt and thus run-off into coastal ecosystems. Seasonal temperature change also remodels the ion channels in the heart of fish to facilitated preserved cardiac function across a range of temperatures. How this seasonal cardiac remodelling impacts vulnerability to pollutants is currently unknown. In this study we accessed the electrical activity of navaga cod (Eleginus nawaga) ventricular cardiomyocytes under the dual influence of seasonal change and varying concentrations of a pervasive PAH pollutant, 3-methylphenanthrene (3-MP). We used whole-cell patch-clamp to elucidate the effect of various doses of 3-MP on action potential (AP) parameters and the main ion currents (I Kr , I K1 , I Na , I Ca) in ventricular cardiomyocytes isolated from navaga cod in winter and summer at the White Sea, close to the Russian Arctic circle. Navaga cod ventricular cardiomyocytes were particularly vulnerable to 3-MP during the winter season. Exposure to 300 nM 3-MP resulted in significant changes in AP duration in winter-acclimatized fish, whereas no such changes were observed in summer-acclimatized fish. The I Kr current was the most sensitive to 3-MP, with a winter IC 50 of 49.7 nM and a summer IC 50 of 53 μM. The I Na current also exhibited seasonal shifts in sensitivity to 3-MP, with IC 50 values of 2.39 μM in winter-acclimatized fish and 7.73 μM in summer-acclimatized fish. No significant differences were observed in the effect of 3-MP on the peak I Ca current, although 3 μM of 3-MP caused a pronounced decrease in charge transferred by I Ca (e.g. Q Ca) in both seasons. The I K1 current was insensitive to 3-MP in both winter and summer fish. These findings highlight how remodelling of the fish heart with changing season alters the potency of PAH pollution. This paper lays the groundwork for future research on the molecular mechanisms that drive the altered seasonal potency of pollutants in navaga cod and other species. [Display omitted] • Seasons impact the bioavailability of pollutants and the complement of ion channels in the heart. • Ion channel remodelling occurred to preserve heart function across temperatures. • As ion channels are the targets of PAH pollution, this seasonal remodelling thus changed cardiac pollution-sensitivity.3MP, was more cardiotoxic in winter than summer fish due potency at IKr. [ABSTRACT FROM AUTHOR]

Abstract: Certain vertebrates, such as freshwater turtles of the genus Chrysemys and Trachemys and crucian carp (Carassius carassius), have anoxia-tolerant hearts that continue to function throughout prolonged periods of anoxia (up to many months) due to successful balancing of cellular ATP supply and demand. In the present review, we summarize the current and limited understanding of the cellular mechanisms underlying this cardiac anoxia tolerance. What emerges is that cold temperature substantially modifies cardiac electrophysiology to precondition the heart for winter anoxia. Intrinsic heart rate is slowed and density of sarcolemmal ion currents substantially modified to alter cardiac action potential (AP) characteristics. These changes depress cardiac activity and reduce the energetic costs associated with ion pumping. In contrast, anoxia per se results in limited changes to cardiac AP shape or ion current densities in turtle and crucian carp, suggesting that anoxic modifications of cardiac electrophysiology to reduce ATP demand are not extensive. Additionally, as knowledge of cellular physiology in non-mammalian vertebrates is still in its infancy, we briefly discuss the cellular defense mechanisms towards the acidosis that accompanies anoxia as well as mammalian cardiac models of hypoxia/ischemia tolerance. By examining if fundamental cellular mechanisms have been conserved during the evolution of anoxia tolerance we hope to have provided a framework for the design of future experiments investigating cardiac cellular mechanisms of anoxia survival. [Copyright &y& Elsevier]

Alkylated polycyclic aromatic hydrocarbons are abundant in crude oil and are enriched during petroleum refinement but knowledge of their cardiotoxicity remains limited. Polycyclic aromatic hydrocarbons (PAHs) are considered the main hazardous components in crude oil and the tricyclic PAH phenanthrene has been singled out for its direct effects on cardiac tissue in mammals and fish. Here we test the impact of the monomethylated phenanthrene, 3-methylphenanthrene (3-MP), on the contractile and electrical function of the atrium and ventricle of a polar fish, the navaga cod (Eleginus nawaga). Using patch-clamp electrophysiology in atrial and ventricular cardiomyocytes we show that 3-MP is a potent inhibitor of the delayed rectifier current I Kr (IC50 = 0.25 μM) and prolongs ventricular action potential duration. Unlike the parent compound phenanthrene, 3-MP did not reduce the amplitude of the L-type Ca2+ current (I Ca) but it accelerated current inactivation thus reducing charge transfer across the myocyte membrane and compromising pressure development of the whole heart. 3-MP was a potent inhibitor (IC50 = 4.7 μM) of the sodium current (I Na), slowing the upstroke of the action potential in isolated cells, slowing conduction velocity across the atrium measured with optical mapping, and increasing atrio-ventricular delay in a working whole heart preparation. Together, these findings reveal the strong cardiotoxic potential of this phenanthrene derivative on the fish heart. As 3-MP and other alkylated phenanthrenes comprise a large fraction of the PAHs in crude oil mixtures, these findings are worrisome for Arctic species facing increasing incidence of spills and leaks from the petroleum industry. 3-MP is also a major component of polluted air but is not routinely measured. This is also of concern if the hearts of humans and other terrestrial animals respond to this PAH in a similar manner to fish. [Display omitted] • 3-MP is a potent inhibitor of I Kr and prolongs action potential duration which is pro-arrhythmic. • Unlike phenanthrene, 3-MP does not cause reduction of I Ca amplitude. • 3-MP greatly accelerates I Ca inactivation, reducing cellular Ca2+-influx and contractile activity of the whole heart. • 3-MP is a potent inhibitor of I Na slowing conduction velocity which is pro-arrhythmic. • More robust environmental monitoring of individual PAHs will improve risk apportionment and inform mitigation policy. [ABSTRACT FROM AUTHOR]

The release of polycyclic aromatic hydrocarbons (PAHs) into the environment due to oil and diesel fuel spills is a serious threat to Arctic fish populations. PAHs produce multiple toxic effects in fish, but disturbance of electrical and contractile activity of the heart seems to be the most negative effect. Our study focused on the effects of fluorene, a tricyclic PAH resembling the well-investigated tricyclic phenanthrene, on major ionic currents and action potential (AP) waveform in isolated ventricular myocytes and on contractile activity in isolated whole hearts of polar navaga cod (Eleginus nawaga). Among the studied currents, the repolarizing rapid delayed rectifier K+ current I Kr demonstrated the highest sensitivity to fluorene with IC50 of 0.54 μM. The depolarizing inward currents, I Na and I CaL , were inhibited with 10 μM fluorene by 20.2 ± 2.8 % and 27.9 ± 8.4 %, respectively, thereby being much less sensitive to fluorene than I Kr. Inward rectifier I K1 current was insensitive to fluorene (up to 10 μM). While 3 μM fluorene prolonged APs, 10 μM also slowed the AP upstroke. Resting membrane potential was not affected by any tested concentrations. In isolated heart experiments 10 μM fluorene caused modest depression of ventricular contractile activity. Thus, we have demonstrated that fluorene, a tricyclic PAH present in high quantities in crude oil, strongly impacts electrical activity with only slight effects on contractile activity in the heart of the polar fish, the navaga cod. [Display omitted] • A polycyclic aromatic hydrocarbon fluorene (Flu) affects navaga fish heart. • In ventricular myocytes Flu strongly inhibits delayed rectifier current I Kr (IC50 = 0.54 μM). • Inhibition of I Kr leads to slowing of repolarization in cardiomyocytes by Flu. • Less efficiently Flu inhibits inward depolarizing currents – I Na and I CaL. • The latter effect leads to moderate depression of myocardial contractility by 10 μM flu. [ABSTRACT FROM AUTHOR]

Catecholamines mediate the 'fight or flight' response in a wide variety of vertebrates. The endogenous catecholamine adrenaline increases heart rate and contractile strength to raise cardiac output. The increase in contractile force is driven in large part by an increase in myocyte Ca2+ influx on the L-type Ca current (I CaL) during the cardiac action potential (AP). Here, we report a K+- based mechanism that prolongs AP duration (APD) in fish hearts following adrenergic stimulation. We show that adrenergic stimulation inhibits the delayed rectifier K+ current (I Kr) in rainbow trout (Oncorhynchus mykiss) cardiomyocytes. This slows repolarization and prolongs APD which may contribute to positive inotropy following adrenergic stimulation in fish hearts. The endogenous ligand, adrenaline (1 μM), which activates both α- and β-ARs reduced maximal I Kr tail current to 61.4 ± 3.9% of control in atrial and ventricular myocytes resulting in an APD prolongation of ~20% at both 50 and 90% repolarization. This effect was reproduced by the α-specific adrenergic agonist, phenylephrine (1 μM), but not the β-specific adrenergic agonist isoproterenol (1 μM). Adrenaline (1 μM) in the presence of β 1 and β 2 -blockers (1 μM atenolol and 1 μM ICI-118551, respectively) also inhibited I Kr. Thus, I Kr suppression following α-adrenergic stimulation leads to APD prolongation in the rainbow trout heart. This is the first time this mechanism has been identified in fish and may act in unison with the well-known enhancement of I CaL following adrenergic stimulation to prolong APD and increase cardiac inotropy. [Display omitted] • Adrenergic stimulation increases action potential duration in the rainbow trout heart. • AP prolongation is mediated by a decrease in I Kr current density following adrenergic stimulation. • This effect appears to be mediated by α-adrenoreceptors. • We confirm earlier work that action potential prolongation occurs due to an increase in extracellular Ca2+ influx on I CaL. [ABSTRACT FROM AUTHOR]

Crustaceans are important ecosystem bio-indicators but their response to pollutants such as polyaromatic hydrocarbons (PAHs) remains understudied, particularly in freshwater habitats. Here we investigated the effect of phenanthrene (at 0.5, 1.0 and 1.5 mg L−1), a 3-ringed PAH associated with petroleum-based aquatic pollution on survival, in vivo and in situ cardiac performance, the oxidative stress response and the tissue burden in the signal crayfish (Pacifastacus leniusculus). Non-invasive sensors were used to monitor heart rate during exposure. Phenanthrene reduced maximum attainable heart rate in the latter half (days 8–15) of the exposure period but had no impact on routine heart rate. At the end of the 15-day exposure period, the electrical activity of the semi-isolated in situ crayfish heart was assessed and significant prolongation of the QT interval of the electrocardiogram was observed. Enzyme pathways associated with oxidative stress (superoxide dismutase and total oxyradical scavenging capacity) were also assessed after 15 days of phenanthrene exposure in gill, hepatopancreas and skeletal muscle; the results suggest limited induction of protective antioxidant pathways. Lastly, we report that 15 days exposure caused a dose-dependent increase in phenanthrene in hepatopancreas and heart tissues which was associated with reduced survivability. To our knowledge, this study is the first to provide such a thorough understanding of the impact of phenanthrene on a crustacean. Image 1 • The 3 ring PAH phenanthrene is common in freshwater systems but its impact on the hearts of crustaceans is unknown. • 15-day phenanthrene exposure impairs maximum heart rate and impacts the electrocardiogram of the signal crayfish. • Phenanthrene induces a limited and tissue-specific response in antioxidant enzymes activity. • Phenanthrene bioaccumulates and decreases survival, possibly due to reduced cardiac function and limited antioxidant defense. [ABSTRACT FROM AUTHOR]