Evidence map›Paper›PMID 26563996›Full record

ArticleNeurotoxicity research2016

The Crucial Involvement of Retinoid X Receptors in DDE Neurotoxicity.

A Wnuk, J Rzemieniec, E Litwa, W Lasoń, W Krzeptowski, A K Wójtowicz, M Kajta

Open access · hybridAbstract read
In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Retinoid X Receptor Antagonists.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Implications of DNA Methylation in Parkinson's Disease.Frontiers in molecular neuroscience · 2017
    Review
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 4 institutions in 1 country.

A WnukDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Kraków, Poland.
J RzemieniecDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Kraków, Poland.
E LitwaDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Kraków, Poland.
W LasońDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Kraków, Poland.
W KrzeptowskiDepartment of Genetics and Evolution, Institute of Zoology, Jagiellonian University, 9 Gronostajowa Street, 30-387, Kraków, Poland.
A K WójtowiczDepartment of Animal Biotechnology, Faculty of Animal Sciences, University of Agriculture, Redzina 1B, 30-248, Kraków, Poland.
M KajtaDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Kraków, Poland. kajta@if-pan.krakow.pl.
Polish Academy of Sciences · PLMaj Institute of Pharmacology · PLJagiellonian University · PLUniversity of Agriculture in Krakow · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dichlorodiphenyldichloroethylene (DDE) is a primary environmental and metabolic degradation product of the pesticide dichlorodiphenyltrichloroethane (DDT). It is one of the most toxic compounds belonging to organochlorines. DDE has never been commercially produced; however, the parent pesticide DDT is still used in some developing countries for disease-vector control of malaria. DDT and DDE remain in the environment because these chemicals are resistant to degradation and bioaccumulate in the food chain. Little is known, however, about DDE toxicity during the early stages of neural development. The results of the present study demonstrate that DDE induced a caspase-3-dependent apoptosis and caused the global DNA hypomethylation in mouse embryonic neuronal cells. This study also provided evidence for DDE-isomer-non-specific alterations of retinoid X receptor α (RXRα)- and retinoid X receptor β (RXRβ)-mediated intracellular signaling, including changes in the levels of the receptor mRNAs and changes in the protein levels of the receptors. DDE-induced stimulation of RXRα and RXRβ was verified using selective antagonist and specific siRNAs. Co-localization of RXRα and RXRβ was demonstrated using confocal microscopy. The apoptotic action of DDE was supported at the cellular level through Hoechst 33342 and calcein AM staining experiments. In conclusion, the results of the present study demonstrated that the stimulation of RXRα- and RXRβ-mediated intracellular signaling plays an important role in the propagation of DDE-induced apoptosis during early stages of neural development.

Indexed as

AnimalsApoptosisBenzoatesBiphenyl CompoundsBrainCaspase 3Cells, CulturedDichlorodiphenyl DichloroethyleneDNA MethylationDose-Response Relationship, DrugEmbryo, MammalianFluoresceinsGene Expression RegulationL-Lactate DehydrogenaseMiceNeuronsBenzoatesBiphenyl Compoundscalcein AMCaspase 3diazepinylbenzoic acidDichlorodiphenyl DichloroethyleneFluoresceinsL-Lactate DehydrogenaseNeurotoxinsRetinoid X ReceptorsRNA, Small InterferingDDEDDTNeurotoxicityPrimary neuronal cell culturesRetinoid X receptorRXR

Identifiers

PMID26563996
PMCPMC4701765
OpenAlexW2249375158

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.