The potential impacts of migratory difficulty, including warmer waters and altered flow conditions, on the reproductive success of salmonid fishes

AbstractClimate 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

3-methyl-phenanthrene (3-MP) disrupts the electrical and contractile activity of the heart of the polar fish, navaga cod (Eleginus nawaga)

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 atria 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 IKr (EC50=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 (ICa) 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 (EC50=4.7 μM) of the sodium current (INa), slowing the upstroke of the action potential in isolated cells, slowing conduction velocity across the atria 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.<br/

Inhibition of the hERG potassium channel by phenanthrene:a polycyclic aromatic hydrocarbon pollutant

The lipophilic polycyclic aromatic hydrocarbon (PAH) phenanthrene is relatively abundant in polluted air and water and can access and accumulate in human tissue. Phenanthrene has been reported to interact with cardiac ion channels in several fish species. This study was undertaken to investigate the ability of phenanthrene to interact with hERG (human Ether-à-go-go-Related Gene) encoded Kv11.1 K(+) channels, which play a central role in human ventricular repolarization. Pharmacological inhibition of hERG can be proarrhythmic. Whole-cell patch clamp recordings of hERG current (I(hERG)) were made from HEK293 cells expressing wild-type (WT) and mutant hERG channels. WT I(hERG1a) was inhibited by phenanthrene with an IC(50) of 17.6 ± 1.7 µM, whilst I(hERG1a/1b) exhibited an IC(50) of 1.8 ± 0.3 µM. WT I(hERG) block showed marked voltage and time dependence, indicative of dependence of inhibition on channel gating. The inhibitory effect of phenanthrene was markedly impaired by the attenuated inactivation N588K mutation. Remarkably, mutations of S6 domain aromatic amino acids (Y652, F656) in the canonical drug binding site did not impair the inhibitory action of phenanthrene; the Y652A mutation augmented I(hERG) block. In contrast, the F557L (S5) and M651A (S6) mutations impaired the ability of phenanthrene to inhibit I(hERG), as did the S624A mutation below the selectivity filter region. Computational docking using a cryo-EM derived hERG structure supported the mutagenesis data. Thus, phenanthrene acts as an inhibitor of the hERG K(+) channel by directly interacting with the channel, binding to a distinct site in the channel pore domain. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00018-021-03967-8

Diesel degradation capability and environmental robustness of strain Pseudomonas aeruginosa WS02

Petroleum hydrocarbon (PHC) degrading bacteria have been frequently discovered. However, in practical application, a single species of PHC degrading bacterium with weak competitiveness may face environmental pressure and competitive exclusion due to the interspecific competition between petroleum-degrading bacteria as well as indigenous microbiota in soil, leading to a reduced efficacy or even malfunction. In this study, the diesel degradation ability and environmental robustness of an endophytic strain Pseudomonas aeruginosa WS02, were investigated. The results show that the cell membrane surface of WS02 was highly hydrophobic, and the strain secreted glycolipid surfactants. Genetic analysis results revealed that WS02 contained multiple metabolic systems and PHC degradation-related genes, indicating that this strain theoretically possesses the capability of oxidizing both alkanes and aromatic hydrocarbons. Gene annotation also showed many targets which coded for heavy metal resistant and metal transporter proteins. The gene annotation-based inference was confirmed by the experimental results: GC-MS analysis revealed that short chain PHCs (C10–C14) were completely degraded, and the degradation of PHCs ranging from C15–C22 were above 90% after 14 d in diesel-exposed culture; Heavy metal (Mn2+, Pb2+ and Zn2+) exposure was found to affect the growth of WS02 to some extent, but not its ability to degrade diesel, and the degradation efficiency was still maintained at 39–59%. WS02 also showed a environmental robustness along with PHC-degradation performance in the co-culture system with other bacterial strains as well as in the co-cultured system with the indigenous microbiota in soil fluid extracted from a PHC-contaminated site. It can be concluded that the broad-spectrum diesel degradation efficacy and great environmental robustness give P. aeruginosa WS02 great potential for application in the remediation of PHC-contaminated soil.<br/

Compliance of the fish outflow tract is altered by thermal acclimation through connective tissue remodelling

From The Royal Society via Jisc Publications RouterHistory: received 2021-06-14, accepted 2021-10-26, collection 2021-11, pub-electronic 2021-11-17Article version: VoRPublication status: PublishedFunder: BBSRCFunder: Leverhulme Trust; Id: http://dx.doi.org/10.13039/501100000275; Grant(s): 240613To protect the gill capillaries from high systolic pulse pressure, the fish heart contains a compliant non-contractile chamber called the bulbus arteriosus which is part of the outflow tract (OFT) which extends from the ventricle to the ventral aorta. Thermal acclimation alters the form and function of the fish atria and ventricle to ensure appropriate cardiac output at different temperatures, but its impact on the OFT is unknown. Here we used ex vivo pressure–volume curves to demonstrate remodelling of passive stiffness in the rainbow trout (Oncorhynchus mykiss) bulbus arteriosus following more than eight weeks of thermal acclimation to 5, 10 and 18°C. We then combined novel, non-biased Fourier transform infrared spectroscopy with classic histological staining to show that changes in compliance were achieved by changes in tissue collagen-to-elastin ratio. In situ gelatin zymography and SDS-PAGE zymography revealed that collagen remodelling was underpinned, at least in part, by changes in activity and abundance of collagen degrading matrix metalloproteinases. Collectively, we provide the first indication of bulbus arteriosus thermal remodelling in a fish and suggest this remodelling ensures optimal blood flow and blood pressure in the OFT during temperature change

Polyaromatic hydrocarbons in pollution: a heart-breaking matter

Air pollution is associated with detrimental effects on human health, including decreased cardiovascular function. However, the causative mechanisms behind these effects have yet to be fully elucidated. Here we review the current epidemiological, clinical and experimental evidence linking pollution with cardiovascular dysfunction. Our focus is on particulate matter (PM) and the associated low molecular weight polycyclic aromatic hydrocarbons (PAHs) as key mediators of cardiotoxicity. We begin by reviewing the growing epidemiological evidence linking air pollution to cardiovascular dysfunction in humans. We next address the pollution‐based cardiotoxic mechanisms first identified in fish following the release of large quantities of PAHs into the marine environment from point oil spills (e.g. Deepwater Horizon). We finish by discussing the current state of mechanistic knowledge linking PM and PAH exposure to mammalian cardiovascular patho‐physiologies such as atherosclerosis, cardiac hypertrophy, arrhythmias, contractile dysfunction and the underlying alterations in gene regulation. Our aim is to show conservation of toxicant pathways and cellular targets across vertebrate hearts to allow a broad framework of the global problem of cardiotoxic pollution to be established. AhR; Aryl hydrocarbon receptor. Dark lines indicate topics discussed in this review. Grey lines indicate topics reviewed elsewhere.publishedVersio

Developmental plasticity of cardiac anoxia-tolerance in juvenile common snapping turtles ( Chelydra serpentina)

Article describes study which tested the hypothesis that developmental hypoxia alters cardiomyocyte physiology in a manner that protects the heart from hypoxic stress