Evidence map›Paper›PMID 24788080›Full record

ArticleScientific reports2014

Developmental toxicity of diclofenac and elucidation of gene regulation in zebrafish (Danio rerio).

Jia-Bin Chen, Hong-Wen Gao, Ya-Lei Zhang, Yong Zhang, Xue-Fei Zhou, Chun-Qi Li, Hai-Ping Gao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 89 citations in OpenAlex.

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  14. Oxidative degradation of diclofenac by thermally activated persulfate: implication for ISCO.Environmental science and pollution research international · 2016
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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 1 country.

Jia-Bin ChenState Key Laboratory of Pollution Control and Resources Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai, 200092, China.
Hong-Wen GaoState Key Laboratory of Pollution Control and Resources Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai, 200092, China.
Ya-Lei ZhangState Key Laboratory of Pollution Control and Resources Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai, 200092, China.
Yong ZhangHunter Biotechnology, Inc., Hangzhou, 311231, China.
Xue-Fei ZhouState Key Laboratory of Pollution Control and Resources Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai, 200092, China.
Chun-Qi LiHunter Biotechnology, Inc., Hangzhou, 311231, China.
Hai-Ping GaoState Key Laboratory of Pollution Control and Resources Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai, 200092, China.
Tongji University · CNState Key Laboratory of Pollution Control and Resource Reuse · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental pollution by emerging contaminants, e.g. pharmaceuticals, has become a matter of widespread concern in recent years. We investigated the membrane transport of diclofenac and its toxic effects on gene expression and the development of zebrafish embryos. The association of diclofenac with the embryos conformed to the general partition model at low concentration, the partition coefficient being 0.0033 ml per embryo. At high concentration, the interaction fitted the Freundlich model. Most of the diclofenac remained in the extracellular aqueous solution with less than 5% interacting with the embryo, about half of which was adsorbed on the membranes while the rest entered the cytoplasm. Concentrations of diclofenac over 10.13 μM were lethal to all the embryos, while 3.78 μM diclofenac was teratogenic. The development abnormalities at 4 day post treatment (dpt) include shorter body length, smaller eye, pericardial and body edema, lack of liver, intestine and circulation, muscle degeneration, and abnormal pigmentation. The portion of the diclofenac transferred into the embryo altered the expression of certain genes, e.g. down-regulation of Wnt3a and Gata4 and up-regulation of Wnt8a. The alteration of expression of such genes or the regulation of downstream genes could cause defects in the cardiovascular and nervous systems.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalDiclofenacEcotoxicologyEmbryonic DevelopmentEmbryo, NonmammalianEnvironmental ExposureEnvironmental PollutantsGene Expression RegulationTime FactorsZebrafishAnti-Inflammatory Agents, Non-SteroidalDiclofenacEnvironmental Pollutants

Identifiers

PMID24788080
PMCPMC4007093
OpenAlexW2049377116

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.