Evidence map›Paper›PMID 31499312›Full record

ArticleChemosphere2020

Understanding the cardiac toxicity of the anthropogenic pollutant phenanthrene on the freshwater indicator species, the brown trout (Salmo trutta): From whole heart to cardiomyocytes.

Martins Oshioriamhe Ainerua, Jake Tinwell, Shiva Nag Kompella, Elin Sørhus, Keith N White, Bart E van Dongen, Holly A Shiels

Open access · hybridAbstract read
In one paragraph

Article in Chemosphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  4. Aryl hydrocarbon receptor-dependent toxicity by retene requires metabolic competence.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 3 countries.

Martins Oshioriamhe AineruaCardiovascular Division, School of Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Core Technology Facility Building, Manchester, M13 9NT, United Kingdom; Department of Animal and Environmental Biology, Faculty of Life Sciences, University of Benin, PMB 1154, Benin City, Nigeria.
Jake TinwellCardiovascular Division, School of Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Core Technology Facility Building, Manchester, M13 9NT, United Kingdom.
Shiva Nag KompellaCardiovascular Division, School of Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Core Technology Facility Building, Manchester, M13 9NT, United Kingdom.
Elin SørhusInstitute of Marine Research, P.O. Box 1870, Nordnes, NO-5817, Bergen, Norway.
Keith N WhiteSchool of Earth Atmospheric and Environmental Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9GB, United Kingdom.
Bart E van DongenSchool of Earth Atmospheric and Environmental Sciences, Williamson Research Centre for Molecular Science, University of Manchester, Williamson Building, Oxford Road, Manchester, M13 9PL, United Kingdom.
Holly A ShielsCardiovascular Division, School of Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Core Technology Facility Building, Manchester, M13 9NT, United Kingdom. Electronic address: Holly.shiels@manchester.ac.uk.
University of Manchester · GBNorwegian Institute of Marine Research · NO

Funding

British Heart Foundation PG/17/77/33125
6 · The paper itself

Abstract

Freshwater systems are faced with a myriad of stressors including geomorphological alterations, nutrient overloading and pollution. Previous studies in marine fish showed polyaromatic hydrocarbons (PAHs) to be cardiotoxic. However, the cardiotoxicity of anthropogenic pollutants in freshwater fishes is unclear and has not been examined across multiple levels of cardiac organization. Here we investigated the effect of phenanthrene (Phe), a pervasive anthropogenic pollutant on a sentinel freshwater species, the brown trout (Salmo trutta). We first examined the electrical activity of the whole heart and found prolongation (∼8.6%) of the QT interval (time between ventricular depolarization and repolarization) of the electrocardiogram (ECG) and prolongation (∼13.2%) of the monophasic action potential duration (MAPD) following ascending doses of Phe. At the tissue level, Phe significantly reduced trabecular force generation by ∼24% at concentration 15 μM and above, suggesting Phe reduces cellular calcium cycling. This finding was supported by florescent microscopy showing a reduction (∼39%) in the intracellular calcium transient amplitude following Phe exposure in isolated brown trout ventricular myocytes. Single-cell electrophysiology was used to reveal the mechanism underlying contractile and electrical dysfunction following Phe exposure. A Phe-dependent reduction (∼38%) in the L-type Ca

Indexed as

AnimalsCardiotoxicityElectrocardiographyFresh WaterMyocytes, CardiacPhenanthrenesTroutWater Pollutants, ChemicalphenanthrenePhenanthrenesWater Pollutants, ChemicalAPbrown troutCardiac action potentialECGElectrophysiologyFishPAHsPoly aromatic hydrocarbonsToxicology

Identifiers

PMID31499312
PMCPMC6857438
OpenAlexW2968500422

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.