Evidence map›Paper›PMID 29129777›Full record

ArticleToxicology and applied pharmacology2018

Trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line.

Elana R Elkin, Sean M Harris, Rita Loch-Caruso

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.9field-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

46 citing papers in PubMed, 59 citations in OpenAlex.

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  13. The Role ofBiomedicines · 2024
    Review
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  15. Article
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  18. Article
  19. Trichloroethylene MetaboliteChemical research in toxicology · 2023
    Article
  20. 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

3 authors at 1 institution in 1 country.

Elana R ElkinDepartment of Environmental Health Sciences, University of Michigan, 1415 Washington Heights, Ann Arbor, MI 48109-2029, USA. Electronic address: elkinela@umich.edu.
Sean M HarrisDepartment of Environmental Health Sciences, University of Michigan, 1415 Washington Heights, Ann Arbor, MI 48109-2029, USA. Electronic address: harrsemi@umich.edu.
Rita Loch-CarusoDepartment of Environmental Health Sciences, University of Michigan, 1415 Washington Heights, Ann Arbor, MI 48109-2029, USA. Electronic address: rlc@umich.edu.
University of Michigan · US

Funding

Research Experiences and Training Coordination CoreP42ES017198 · NIEHS · NORTHEASTERN UNIVERSITY · PI ALSHAWABKEH, AKRAM N · 2010 to 2024
$38.6M
Strategic Vision & Impact on Environmental HealthP30ES017885 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Dana Dolinoy · 2011 to 2026
$21.3M
ENVIRONMENTAL TOXICOLOGY PRE/POST DOCTORAL RES.TRAININGT32ES007062 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Justin Adam Colacino · 1985 to 2026
$10.5M
NIEHS NIH HHS P30 ES017885NIEHS NIH HHS P42 ES017198NIEHS NIH HHS T32 ES007062
6 · The paper itself

Abstract

Trichloroethylene (TCE), a prevalent environmental contaminant, is a potent renal and hepatic toxicant through metabolites such as S-(1, 2-dichlorovinyl)-l-cysteine (DCVC). However, effects of TCE on other target organs such as the placenta have been minimally explored. Because elevated apoptosis and lipid peroxidation in placenta have been observed in pregnancy morbidities involving poor placentation, we evaluated the effects of DCVC exposure on apoptosis and lipid peroxidation in a human extravillous trophoblast cell line, HTR-8/SVneo. We exposed the cells in vitro to 10-100μM DCVC for various time points up to 24h. Following exposure, we measured apoptosis using flow cytometry, caspase activity using luminescence assays, gene expression using qRT-PCR, and lipid peroxidation using a malondialdehyde quantification assay. DCVC significantly increased apoptosis in time- and concentration-dependent manners (p<0.05). DCVC also significantly stimulated caspase 3, 7, 8 and 9 activities after 12h (p<0.05), suggesting that DCVC stimulates the activation of both the intrinsic and extrinsic apoptotic signaling pathways simultaneously. Pre-treatment with the tBID inhibitor Bl-6C9 partially reduced DCVC-stimulated caspase 3 and 7 activity, signifying crosstalk between the two pathways. Additionally, DCVC treatment increased lipid peroxidation in a concentration-dependent manner. Co-treatment with the antioxidant peroxyl radical scavenger (±)-α-tocopherol attenuated caspase 3 and 7 activity, suggesting that lipid peroxidation mediates DCVC-induced apoptosis in extravillous trophoblasts. Our findings suggest that DCVC-induced apoptosis and lipid peroxidation in extravillous trophoblasts could contribute to poor placentation if similar effects occur in vivo in response to TCE exposure, indicating that further studies into this mechanism are warranted.

Indexed as

ApoptosisCaspase 3Caspase 7Cell Cycle ProteinsCells, CulturedCysteineFemaleGADD45 ProteinsHumansLipid PeroxidationNF-kappa B p50 SubunitNuclear ProteinsPlacentaPregnancyPregnancy Trimester, FirstReactive Oxygen SpeciesCaspase 3Caspase 7Cell Cycle ProteinsCysteineGADD45A protein, humanGADD45 ProteinsNF-kappa B p50 SubunitNFKB1 protein, humanNuclear ProteinsReactive Oxygen SpeciesS-(1,2-dichlorovinyl)cysteineApoptosisExtravillous trophoblastsLipid peroxidationPlacentaS-(1,2-dichlorovinyl)-l-cysteine [DCVC]Trichloroethylene [TCE]

Identifiers

PMID29129777
PMCPMC5741094
OpenAlexW2767755936

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.