Evidence map›Paper›PMID 36446765›Full record

ArticleCell death & disease2022

p53 triggers mitochondrial apoptosis following DNA damage-dependent replication stress by the hepatotoxin methyleugenol.

Max J Carlsson, Anastasia S Vollmer, Philipp Demuth, Daniel Heylmann, Diana Reich, Caroline Quarz, Birgit Rasenberger, Teodora Nikolova, Thomas G Hofmann, Markus Christmann and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 41 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

15 authors at 3 institutions in 1 country.

Max J Carlsson *Division of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Anastasia S Vollmer *Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, 35392, Giessen, Germany.
Philipp DemuthDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Daniel HeylmannRudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, 35392, Giessen, Germany.
Diana ReichInstitute of Toxicology, University Medical Center, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Caroline QuarzDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Birgit RasenbergerInstitute of Toxicology, University Medical Center, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Teodora NikolovaInstitute of Toxicology, University Medical Center, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Thomas G HofmannInstitute of Toxicology, University Medical Center, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.ORCID 0000-0003-0547-2720
Markus ChristmannInstitute of Toxicology, University Medical Center, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Julia A FuhlbrueckDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Simone StegmüllerDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Elke RichlingDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Alexander T CartusDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany.
Jörg FahrerDivision of Food Chemistry and Toxicology, Department of Chemistry, Technical University of Kaiserslautern, 67663, Kaiserslautern, Germany. fahrer@chemie.uni-kl.de.ORCID 0000-0001-5225-2718
University of Kaiserslautern · DEJohannes Gutenberg University Mainz · DEJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer is one of the most frequent tumor entities worldwide, which is causally linked to viral infection, fatty liver disease, life-style factors and food-borne carcinogens, particularly aflatoxins. Moreover, genotoxic plant toxins including phenylpropenes are suspected human liver carcinogens. The phenylpropene methyleugenol (ME) is a constituent of essential oils in many plants and occurs in herbal medicines, food, and cosmetics. Following its uptake, ME undergoes Cytochrome P450 (CYP) and sulfotransferase 1A1 (SULT1A1)-dependent metabolic activation, giving rise to DNA damage. However, little is known about the cellular response to the induced DNA adducts. Here, we made use of different SULT1A1-proficient cell models including primary hepatocytes that were treated with 1'-hydroxymethyleugenol (OH-ME) as main phase I metabolite. Firstly, mass spectrometry showed a concentration-dependent formation of N

Indexed as

DNA AdductsTumor Suppressor Protein p53Apoptosisbcl-2-Associated X ProteinCarcinogensDNA DamageEugenolHumans1'-(hydroxymethyl)eugenolbcl-2-Associated X ProteinCarcinogensDNA AdductsEugenolmethyleugenolTumor Suppressor Protein p53

Identifiers

PMID36446765
PMCPMC9708695
OpenAlexW4310600670

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.