Evidence map›Paper›PMID 29518658›Full record

ArticleEnvironmental pollution (Barking, Essex : 1987)2018

In vitro profiling of toxic effects of prominent environmental lower-chlorinated PCB congeners linked with endocrine disruption and tumor promotion.

Kateřina Pěnčíková, Lucie Svržková, Simona Strapáčová, Jiří Neča, Iveta Bartoňková, Zdeněk Dvořák, Martina Hýžďalová, Jakub Pivnička, Lenka Pálková, Hans-Joachim Lehmler and 3 more

Abstract read
In one paragraph

Article in Environmental pollution (Barking, Essex : 1987), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 74 citations in OpenAlex.

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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

13 authors at 5 institutions in 2 countries.

Kateřina PěnčíkováDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic.
Lucie SvržkováDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic.
Simona StrapáčováDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic.
Jiří NečaDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic.
Iveta BartoňkováDepartment of Cell Biology and Genetics, Faculty of Science, Šlechtitelů 11, Palacký University, 78371 Olomouc, Czech Republic.
Zdeněk DvořákDepartment of Cell Biology and Genetics, Faculty of Science, Šlechtitelů 11, Palacký University, 78371 Olomouc, Czech Republic.
Martina HýžďalováDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic; Department of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 61265 Brno, Czech Republic.
Jakub PivničkaDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 61265 Brno, Czech Republic.
Lenka PálkováDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic.
Hans-Joachim LehmlerDepartment of Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, 52242, IA, USA.
Xueshu LiDepartment of Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, 52242, IA, USA.
Jan VondráčekDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 61265 Brno, Czech Republic. Electronic address: vondracek@ibp.cz.
Miroslav MachalaDepartment of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 70, 62100 Brno, Czech Republic. Electronic address: machala@vri.cz.
Veterinary Research Institute · CZCzech Academy of Sciences, Institute of Biophysics · CZPalacký University Olomouc · CZUniversity of Iowa · USCzech Academy of Sciences · CZ

Funding

Training CoreP42ES013661 · NIEHS · UNIVERSITY OF IOWA · PI Rachel Frances Marek · 2006 to 2026
$60.3M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
NIEHS NIH HHS P30 ES005605NIEHS NIH HHS P42 ES013661
6 · The paper itself

Abstract

The mechanisms contributing to toxic effects of airborne lower-chlorinated PCB congeners (LC-PCBs) remain poorly characterized. We evaluated in vitro toxicities of environmental LC-PCBs found in both indoor and outdoor air (PCB 4, 8, 11, 18, 28 and 31), and selected hydroxylated metabolites of PCB 8, 11 and 18, using reporter gene assays, as well as other functional cellular bioassays. We focused on processes linked with endocrine disruption, tumor promotion and/or regulation of transcription factors controlling metabolism of both endogenous compounds and xenobiotics. The tested LC-PCBs were found to be mostly efficient anti-androgenic (within nanomolar - micromolar range) and estrogenic (at micromolar concentrations) compounds, as well as inhibitors of gap junctional intercellular communication (GJIC) at micromolar concentrations. PCB 8, 28 and 31 were found to partially inhibit the aryl hydrocarbon receptor (AhR)-mediated activity. The tested LC-PCBs were also partial constitutive androstane receptor (CAR) and pregnane X receptor (PXR) agonists, with PCB 4, 8 and 18 being the most active compounds. They were inactive towards other nuclear receptors, such as vitamin D receptor, thyroid receptor α, glucocorticoid receptor or peroxisome proliferator-activated receptor γ. We found that only PCB 8 contributed to generation of oxidative stress, while all tested LC-PCBs induced arachidonic acid release (albeit without further modulations of arachidonic acid metabolism) in human lung epithelial cells. Importantly, estrogenic effects of hydroxylated (OH-PCB) metabolites of LC-PCBs (4-OH-PCB 8, 4-OH-PCB 11 and 4'-OH-PCB 18) were higher than those of the parent PCBs, while their other toxic effects were only slightly altered or suppressed. This suggested that metabolism may alter toxicity profiles of LC-PCBs in a receptor-specific manner. In summary, anti-androgenic and estrogenic activities, acute inhibition of GJIC and suppression of the AhR-mediated activity were found to be the most relevant modes of action of airborne LC-PCBs, although they partially affected also additional cellular targets.

Indexed as

Air PollutantsCell LineConstitutive Androstane ReceptorEndocrine DisruptorsEpithelial CellsHumansHydroxylationNeoplasmsPolychlorinated BiphenylsPregnane X ReceptorReceptors, Cytoplasmic and NuclearReceptors, SteroidSignal TransductionAir PollutantsConstitutive Androstane ReceptorEndocrine DisruptorsPolychlorinated BiphenylsPregnane X ReceptorReceptors, Cytoplasmic and NuclearReceptors, SteroidAirborne polychlorinated biphenylsEndocrine disruptionHydroxyLated PCBsMetabolism of xenobioticsTumor promotion

Identifiers

PMID29518658
PMCPMC5908724
OpenAlexW2791452042

What OpenQuestion holds

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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.