Evidence map›Paper›PMID 31294873›Full record

ArticleEnvironmental and molecular mutagenesis2019

Mode-of-action analysis of the effects induced by nicotine in the in vitro micronucleus assay.

Daniel J Smart, Fabian R Helbling, Maëlle Verardo, Damian McHugh, Patrick Vanscheeuwijck

Open access · hybridAbstract read
In one paragraph

Article in Environmental and molecular mutagenesis, 2019. 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
0.8field-weighted citation impact, top 34% 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, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Genotoxic potential of a novel PDE-4B inhibitor Apremilast by chromosomal aberration and micronucleus assay in mice.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
    Article
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

5 authors at 1 institution in 1 country.

Daniel J SmartPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.ORCID 0000-0002-7531-3584
Fabian R HelblingPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Maëlle VerardoPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Damian McHughPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Patrick VanscheeuwijckPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Philip Morris International (Switzerland) · CH

Funding

Philip Morris International
6 · The paper itself

Abstract

Nicotine's genotoxic potential has been extensively studied in vitro. While the results of mammalian cell-based studies have inferred that it can potentially damage chromosomes, in general and with few exceptions, adverse DNA effects have been observed primarily at supraphysiological concentrations in nonregulatory assays that provide little information on its mode-of-action (MoA). In this study, a modern-day regulatory genotoxicity assessment was conducted using a flow cytometry-based in vitro micronucleus (MN) assay, Good Laboratory Practice study conditions, Chinese hamster ovary cells of known provenance, and acceptance/evaluation criteria from the current OECD Test Guideline 487. Nicotine concentrations up to 3.95 mM had no effect on background levels of DNA damage; however, concentrations above the point-of-departure range of 3.94-4.54 mM induced increases in MN and hypodiploid nuclei, indicating a possible aneugenicity hazard. Follow-up experiments designed to elucidate nicotine's MoA revealed cellular vacuolization, accompanying distortions in microtubules, inhibition of tubulin polymerization, centromere-positive DNA, and multinucleate cells at MN-inducing concentrations. Vacuoles likely originated from acidic cellular compartments (e.g., lysosomes). Remarkably, genotoxicity was suppressed by chemicals that raised the luminal pH of these organelles. Other endpoints (e.g., changes in phosphorylated histones) measured in the study cast doubt on the biological relevance of this apparent genotoxicity. In addition, three major nicotine metabolites, including cotinine, had no MN effects but nornicotine induced a nicotine-like profile. It is possible that nicotine's lysosomotropic properties drive the genotoxicity observed in vitro; however, the potency and mechanistic insights revealed here indicate that it is likely of minimal physiological relevance for nicotine consumers. Environ. Mol. Mutagen. 2019. © 2019 The Authors. Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society.

Indexed as

AneugensAnimalsCell LineCell NucleusCHO CellsCricetulusDNADNA DamageMicronucleus TestsMicrotubulesMutagenicity TestsMutagensNicotinePhosphorylationTubulinAneugensDNAMutagensNicotinenornicotineTubulinaneugenicitygenotoxic mechanismlysosomotropism

Identifiers

PMID31294873
PMCPMC6900147
OpenAlexW2957688932

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.