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Replication Data for: Parker et al. Mechanisms of PVP-functionalized silver nanoparticle toxicity in fish: Intravascular exposure disrupts cardiac pacemaker function and inhibits Na+/K+-ATPase activity in heart, but not gill
No full textReplication data for: Parker, K.S., El, N., Buldo, E.C., MacCormack, T.J. Mechanisms of PVP-functionalized silver nanoparticle toxicity in fish: Intravascular exposure disrupts cardiac pacemaker function and inhibits Na+/K+-ATPase activity in heart, but not gill.
The goal of this study was to determine if polyvinylpyrrolidone-functionalized silver nanoparticles influence the control of heart rate, blood pressure, or cardiac Na+/K+-ATPase activity in vivo in brook trout
Nanotoxicology: The impacts of 5 nm silver nanoparticles on protein synthesis of rainbow trout (oncorhynchus mykiss)
Full text linkSilver nanoparticles (nAg) are becoming increasingly prevalent in consumer products due
to their unique physicochemical properties. This excessive usage is causing nanoparticulate waste
to end up in the water column with the potential to affect aquatic organisms. Previous research has
shown damaging effects of engineered nanomaterials (ENMs) on various fish species with the
current study aimed to identify the impacts of polyvinyl pyrrolidone (PVP) capped 5 nm silver
nanoparticles on biochemical stress indicators and rates of protein synthesis in rainbow trout
(Oncorhynchus mykiss). Fish were exposed to 100 μg L-1 nAg or 0.22 μg L-1 AgNO3 for 48 hours
and tissue samples taken. Biological endpoints analyzed included hematocrit, gill sodium
potassium ATPase, heart acetylcholinesterase, and cortisol and malondialdehyde content.
Fractional rates of protein synthesis were determined by flooding dose method modified to use a
stable phenylalanine isotope tracer. No significant differences were observed between treatment
groups for any of the biologically relevant endpoints nor protein synthesis rates, although a
decreasing trend was observed for sodium potassium ATPase activity in nAg-exposed fish. Results
suggest that rainbow trout exposed to silver ENMs for 48 hours at the environmentally relevant
point-source exposure concentration tested are not expressing signs of significant damage nor
exhibiting impaired metabolism indicating that under short term conditions 5 nm PVP-capped nAg
at 100 μg L-1 is not acutely toxic. These findings are disputable as previous research has
demonstrated the toxic effects of ENMs on fish physiology, including on the endpoints analyzed
in this study. These results should encourage further research into longer exposure durations and
investigating other potential sublethal effects
The effect of a taurine deficiency on the cardiovascular response of brook char (Salvelinus fontinalis) to hypoxia
Full text linkTaurine is a non-proteogenic β-amino acid found in relatively high abundance within the heart of freshwater teleosts. By exhibiting cardioprotective properties through participation in osmoregulation and calcium (Ca2+) homeostasis, taurine has been linked to supporting the cardiovascular physiology under environmental hypoxia. The functional capacity of the heart is defined by cardiac output (Q ), representing the product of heart rate (fh) and stroke volume (SV). A taurine deficiency has been shown to impair the ability to increase SV under hypoxia in vitro and cause a shorter time to loss of equilibrium (LOE) in vivo, indicating cardiovascular disturbances. The knowledge gap addressed in this study is the effect of a taurine deficiency on all three cardiac parameters in vivo under hypoxia. These measurements were paired with metrics of the O2 carrying capacity of the blood and osmotic stress following acute hypoxia and recovery. Brook char (Salvelinus fontinalis) were used as a representative freshwater teleost, for this analysis. A taurine-deficient (TD) model was achieved through 5% dietary β-alanine supplementation, a known competitive inhibitor of taurine transport. fh, SV, and Q in vivo were quantified using electrocardiograms (ECG) and ultrasonic flows. Significance was found in lower resting fh and blunted bradycardia in TD fish. SV was maintained at similar levels to control fish, although TD fish did not elevate SV under hypoxia, likely tied to their lesser bradycardia. Q was similar in both models, along with hematological parameters characterizing the capacity to transport O2 in circulation. TD hearts had decreased lactate levels, an important metabolite to cardiovascular function under a hypoxia stressor. The main finding of this study is that TD fish have a greater sensitivity to environmental hypoxia, attributed to just a 21% reduction in cardiac taurine. With the typical increase in SV seen under hypoxia attributed to a lower fh, regulatory disruption of contractile frequency may explain the observed physiological differences. As an important mechanism to mitigate osmotic disturbances under hypoxia, a limited ability to perform taurine efflux may be the underlying cause of cardiac dysfunction. This may additionally lead to alterations to the Ca2+current (ICa) acting on the heart's pacemaker or autonomic nervous system activation. With the progression of global warming and v associated disturbances to aquatic O2 availability, ensuring sufficient taurine in the diets of freshwater fish could be a method of supporting cardiovascular function
Cardiac taurine deficiency impairs physiological performance and mitochondrial function in brook trout (Salvelinus fontinalis)
Full text linkTaurine is a nonessential amino acid abundant in skeletal and cardiac muscle tissues. Taurine plays a critical role in many physiological processes, such as osmoregulation, cardioprotection, and oxidative stress mediation. Studies in other animal models have shown that taurine deficiency is associated with the progression of cardiovascular and mitochondrial diseases, as well as interruptions in energy metabolism. This study evaluated the effects of taurine on the physiological performance and mitochondrial function in brook trout, Salvelinus fontinalis. Dietary supplementation of -alanine, a competitive inhibitor of the taurine transporter, was administered over a minimum time frame of four weeks to decrease intracellular taurine concentrations. Two treatment groups were used in this study, a group of fish fed a control diet and a taurine-deficient (TD) group fed the same diet infused with 5% -alanine. The physiological impacts of taurine deficiency were assessed through evaluating the critical thermal maximum (CTmax) and tolerance to acute hypoxia through time-to-loss of equilibrium (LOE) tests. CTmax was evaluated by increasing tank water temperature at a set ramp rate until fish could no longer maintain equilibrium. CTmax was found to be significantly higher in (p=0.017), while tolerance to acute hypoxia was observed to be significantly lower (p=0.015) in TD trout than in the control group. FluoRespirometry evaluated mitochondrial efficiency at different points along the electron transport chain. Increased mitochondrial leak rates were observed in TD trout, indicating a greater degree of proton leak into the intermembrane space (p=0.0056). Activities of mitochondrial complexes I and II were not affected by TD. The average respiratory control ratio (RCR) of the TD trout was significantly decreased in comparison to the control group, indicating that a greater portion of oxygen consumption in TD mitochondria is not coupled with ADP phosphorylation and is instead dissipated as heat energy (p=0.0051). Respirometry also revealed that maximum oxygen consumption of complex IV of the electron transport chain was significantly decreased by TD (p=0.0216). Expression of complex IV protein COX3 was significantly downregulated in TD cardiac muscle tissue, indicating potential defects in protein synthesis correlated with TD (p=0.007). Our findings provide further insight into the roles of taurine, and pathology of taurine deficiency in the cardiovascular system of fish. This understanding can enable us to further gauge the effects of environmental fluctuations on this species
Fish in hot water: effects on taurine on the thermal sensitivity of aerobic metabolism
Full text linkEvaluating the toxicity of silver nanoparticles on the behaviour and and physiology of bristlenose catfish (Ancistrus cirrhosis)
Full text linkSilver nanoparticles (AgNPs) are a common material found in many household items, but as these items are thrown out, AgNPs can leach into the aquatic environment, and are currently being found in increasingly higher concentrations in our water supply. In the aquatic environment, AgNPs aggregate and fall to the bottom, affecting benthic creatures. In this study, the Bristlenose Catfish (Ancistrus Cirrhosis) was used for their benthic nature and their ability to air breathe using their highly vascularized stomachs. By analyzing air breathing frequency (seen only in times of stress), we can better understand what role AgNPs play in a catfish’s ability to tolerate environmental stress. Experimentation was done by isolating catfish for seven days with the absence or presence of AgNPs. On the eighth day, these fish were exposed to one of three environmental conditions: control (optimal conditions), hypoxia (20% O2 saturation), and high temperature (32°C). These fish then had their movement tracked and quantified over 6 hours. In addition to this, fish were placed in a respirometer to measure oxygen consumption, gills were analyzed via scanning electron microscopy, and gut samples were used to determine malondialdehyde (MDA) concentration. It was found that fish regardless of environmental stressor or AgNP presence total distance moved did not change. However, hypoxic fish exposed to AgNPs were found to increase air breathing frequency. This indicates that any movement the catfish is doing is focused on air breathing, which could increase their exposure to aerial predators. Respirometry analysis showed an increase
in oxygen consumption only when AgNPs are present, which is in keeping with behavioral data, since an increase in basal oxygen consumption would lead to a higher air breathing frequency. MDA levels varied between environmental stressors in AgNP exposed fish, but qualitative gill analysis indicated that the gills were not damaged from nanoparticles. Together, these results support our hypotheses that AgNPs do interfere with a catfish’s ability to tolerate environmental stress. It is expected that with an increase in concentration or exposure times, these effects would increase proportionally
The effect of taurine depletion on the cardiovascular system in Salvelinus fontinalis (brook trout)
Full text linkTaurine is a naturally existing β-amino acid found in high concentration in vertebrate cardiomyocytes and contributes to a diversity of cardioregulatory functions. Taurine fluctuations in mammals are quite uncommon because of the absence of osmotic challenges. Contrastingly, fish experience these osmotic imbalances and taurine’s ability to regulate cell volume may play an essential role in these species. Efficient cardiac cycling is essential to the growth and survival of a species in stress and non-stress environments. A decline in intracellular taurine levels has been associated with a decline in the cardiac muscle’s ability to maintain normal function under hypoxia-induced stress. Although poorly understood in teleosts, taurine has been identified as an essential amino acid in mediating Ca2+handling, reducing oxidative stress and acting as an osmoregulator. The main goal of this study is to determine the effects of taurine depletion on the cardiovascular system in brook trout (Salvelinus fontinalis).
We addressed this gap in knowledge by creating two experimental groups, one fed with a 5% β-alanine supplemented feed to inhibit intracellular taurine concentrations and a control fed group. These groups were further analyzed under control and hypoxic conditions. Utilizing an invitro perfused heart preparation, we saw that cardiac function was significantly impaired. Taurine deficient (TD) hearts had significantly lower power outputs whereas there were no significant differences in cardiac output, stroke volume or muscle contractility in TD hearts under oxygenation indicating that heart function was unaffected under optimal conditions. Although in TD hearts we observed significant decreases in cardiac output, stoke volume and power output under hypoxia and even reoxygenation. Taurine deficiency had no direct effects on muscle contractility but was significantly affected by hypoxia and reoxygenation. Previous studies have shown that cardiac taurine deficiency reduced sarcoplasmic reticular Ca2+-ATPase activity affecting contractility in mammals and this effect translates in our brook trout model.
Oxidative stress was significantly decreased in TD hearts compared to the control hearts under both oxygenation and hypoxic reoxygenation. Previous studies that show mitochondrial uncoupling in TD hearts in brook trout may provide the basis to understand this proposed antioxidant effect of taurine deficiency. Intracellular taurine is clearly important to support cardiac performance and stress tolerance in fish. The OCLTT hypothesis suggests that cardiac performance determines upper stress tolerance limits in fish. With the current threat of climate change, taurine supplementation may protect heart function and promote survival
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
ATP-sensitive potassium channels (Katp) in fish cardiac muscle during anoxia and recovery
No full textCardiac muscle from anoxia tolerant and intolerant fishes was used to investigate the importance of ATP-sensitive potassium channels (KATP) in the control of anaerobic cardiac function. KATP channels contribute to anaerobic cardioprotection in mammals yet little is known of their action in more hypoxia tolerant animals. Isometrically contracting ventricular muscle preparations were used to study sarcolemmal and mitochondrial KATP channel activity in the myocardium of three species of teleost fishes (Lipossarcus pardalis'm Limanda ferruginea. and Gadus morhua) with varying cardiac hypoxia tolerances. Channel activity was assessed pharmacologically using the non-specific KATP channel blocker glibenclamide, the mitochondrial specific blocker 5-hydroxydecanoic acid and the agonist, diazoxide to determine the involvment of KATP channels in anaerobic cardiac performance. Results suggest that cardiac KATP channels from hypoxia tolerant fishes are tonically active, resulting in a constant cardioprotection similar to the preconditioned state which can be induced by various methods in mammalian hearts. These studies clearly show that KATP channels are important for anaerobic cardiac function in anoxia tolerant fish.Includes bibliographical references
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