Evidence map›Paper›PMID 34572016›Full record

ArticleCells2021

The Emerging Plasticizer Alternative DINCH and Its Metabolite MINCH Induce Oxidative Stress and Enhance Inflammatory Responses in Human THP-1 Macrophages.

Alexandra Schaffert, Josi Arnold, Isabel Karkossa, Matthias Blüher, Martin von Bergen, Kristin Schubert

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. 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
2.0field-weighted citation impact, top 14% 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.

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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

6 authors at 1 institution in 1 country.

Alexandra SchaffertDepartment of Molecular Systems Biology, Helmholtz-Centre for Environmental Research (UFZ), 04318 Leipzig, Germany.
Josi ArnoldDepartment of Molecular Systems Biology, Helmholtz-Centre for Environmental Research (UFZ), 04318 Leipzig, Germany.
Isabel KarkossaDepartment of Molecular Systems Biology, Helmholtz-Centre for Environmental Research (UFZ), 04318 Leipzig, Germany.ORCID 0000-0003-2781-1877
Matthias BlüherHelmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), 04318 Leipzig, Germany.
Martin von BergenDepartment of Molecular Systems Biology, Helmholtz-Centre for Environmental Research (UFZ), 04318 Leipzig, Germany.
Kristin SchubertDepartment of Molecular Systems Biology, Helmholtz-Centre for Environmental Research (UFZ), 04318 Leipzig, Germany.ORCID 0000-0003-4365-084X
Helmholtz Centre for Environmental Research · DE

Funding

Deutsche Bundesstiftung Umwelt 20017/525Deutsche Forschungsgemeinschaft 209933838Helmholtz-Zentrum für Umweltforschung ProMetheus
6 · The paper itself

Abstract

The use of the plasticizer bis(2-ethylhexyl)phthalate (DEHP) and other plasticizers in the manufacture of plastic products has been restricted due to adverse health outcomes such as obesity, metabolic syndrome, and asthma, for which inflammation has been described to be a driving factor. The emerging alternative plasticizer 1,2-cyclohexanedioic acid diisononyl ester (DINCH) still lacks information regarding its potential effects on the immune system. Here, we investigated the effects of DINCH and its naturally occurring metabolite monoisononylcyclohexane-1,2-dicarboxylic acid ester (MINCH) on the innate immune response. Human THP-1 macrophages were exposed to 10 nM-10 μM DINCH or MINCH for 4 h, 16 h, and 24 h. To decipher the underlying mechanism of action, we applied an untargeted proteomic approach that revealed xenobiotic-induced activation of immune-related pathways such as the nuclear factor κB (NF-κB) signaling pathway. Key drivers were associated with oxidative stress, mitochondrial dysfunction, DNA damage repair, apoptosis, and autophagy. We verified increased reactive oxygen species (ROS) leading to cellular damage, NF-κB activation, and subsequent TNF and IL-1β release, even at low nM concentrations. Taken together, DINCH and MINCH induced cellular stress and pro-inflammatory effects in macrophages, which may lead to adverse health effects.

Indexed as

ApoptosisDicarboxylic AcidsDNA DamageDNA RepairEstersHumansInflammationMacrophagesNF-kappa BOxidative StressPhthalic AcidsPlasticizersProteomicsSignal TransductionTHP-1 CellsDicarboxylic AcidsEstersNF-kappa Bphthalic acidPhthalic AcidsPlasticizersDINCHimmunotoxicitymacrophageplasticizerproteomics

Identifiers

PMID34572016
PMCPMC8466537
OpenAlexW3198280675

What OpenQuestion holds

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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.