Evidence map›Paper›PMID 34040527›Full record

ArticleFrontiers in pharmacology2021

Association of NQO2 With UDP-Glucuronosyltransferases Reduces Menadione Toxicity in Neuroblastoma Cells.

Monivan Chhour, Pierre Perio, Regis Gayon, Hélène Ternet-Fontebasso, Gilles Ferry, Françoise Nepveu, Jean A Boutin, Jan Sudor, Karine Reybier

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Bioactive compounds ofFrontiers in microbiology · 2022
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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

9 authors at 4 institutions in 1 country.

Monivan ChhourPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Pierre PerioPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Regis GayonFlash Therapeutics, Parc Technologique du Canal, Toulouse, France.
Hélène Ternet-FontebassoPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Gilles FerryBiotechnologie, Pharmacologie Moléculaire et Cellulaire, Institut de Recherches Servier, Croissy-sur-Seine, France.
Françoise NepveuPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Jean A BoutinPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Jan SudorPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Karine ReybierPharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France.
Institut de Recherche pour le Développement · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FRUniversité Toulouse III - Paul Sabatier · FRInstitut de Pharmacologie Moléculaire et Cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The balance between detoxification and toxicity is linked to enzymes of the drug metabolism Phase I (cytochrome P450 or oxidoreductases) and phase II conjugating enzymes (such as the UGTs). After the reduction of quinones, the product of the reaction, the quinols-if not conjugated-re-oxidizes spontaneously to form the substrate quinone with the concomitant production of the toxic reactive oxygen species (ROS). Herein, we documented the modulation of the toxicity of the quinone menadione on a genetically modified neuroblastoma model cell line that expresses both the quinone oxidoreductase 2 (NQO2, E.C. 1.10.5.1) alone or together with the conjugation enzyme UDP-glucuronosyltransferase (UGT1A6, E.C. 2.4.1.17), one of the two UGT isoenzymes capable to conjugate menadione. As previously shown, NQO2 enzymatic activity is concomitant to massive ROS production, as previously shown. The quantification of ROS produced by the menadione metabolism was probed by electron-paramagnetic resonance (EPR) on cell homogenates, while the production of superoxide was measured by liquid chromatography coupled to mass spectrometry (LC-MS) on intact cells. In addition, the dysregulation of the redox homeostasis upon the cell exposure to menadione was studied by fluorescence measurements. Both EPR and LCMS studies confirmed a significant increase in the ROS production in the NQO2 overexpressing cells due to the fast reduction of quinone into quinol that can re-oxidize to form superoxide radicals. However, the effect of NQO2 inhibition was drastically different between cells overexpressing only NQO2 vs. both NQO2 and UGT. Whereas NQO2 inhibition decreases the amount of superoxide in the first case by decreasing the amount of quinol formed, it increased the toxicity of menadione in the cells co-expressing both enzymes. Moreover, for the cells co-expressing QR2 and UGT the homeostasis dysregulation was lower in presence of menadione than for the its counterpart expressing only QR2. Those results confirmed that the cooperation of the two enzymes plays a fundamental role during the cells' detoxification process. The fluorescence measurements of the variation of redox homeostasis of each cell line and the detection of a glucuronide form of menadiol in the cells co-expressing NQO2 and UGT1A6 enzymes further confirmed our findings.

Indexed as

cellular toxicityconjugationglucuronidemenadiolNQO2UGT1A6

Identifiers

PMID34040527
PMCPMC8142080
OpenAlexW3163374248

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Registered trials

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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.