Evidence map›Paper›PMID 20030412›Full record

ArticleChemical research in toxicology2010

Chronic exposure to zinc chromate induces centrosome amplification and spindle assembly checkpoint bypass in human lung fibroblasts.

Amie L Holmes, Sandra S Wise, Stephen C Pelsue, AbouEl-Makarim Aboueissa, Wilma Lingle, Jeffery Salisbury, Jamie Gallagher, John Pierce Wise

Open access · greenAbstract read
In one paragraph

Article in Chemical research in toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 28% 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, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Particulate Hexavalent Chromium Inhibits E2F1 Leading to Reduced RAD51 Nuclear Foci Formation in Human Lung Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  12. Article
  13. Prolonged exposure to particulate Cr(VI) is cytotoxic and genotoxic to fin whale cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Prolonged Particulate Hexavalent Chromium Exposure Suppresses Homologous Recombination Repair in Human Lung Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2016
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Amie L HolmesWise Laboratory of Environmental and Genetic Toxicology, Maine Center for Toxicology and Environmental Health, Department of Applied Medical Science, University of Southern Maine, 96 Falmouth Street, Portland, Maine 04104-9300, USA.
Sandra S Wise
Stephen C Pelsue
AbouEl-Makarim Aboueissa
Wilma Lingle
Jeffery Salisbury
Jamie Gallagher
John Pierce Wise
Mayo Clinic · USUniversity of Southern Maine · US

Funding

PARTICULATE CR(VI) TOXICOLOGY IN HUMAN LUNG EPITHELIAL CELLS AND FIBROBLASTS (Admin Supplement/PA-17-055)R01ES016893 · NIEHS · UNIVERSITY OF SOUTHERN MAINE · PI WISE, JOHN PIERCE · 2009 to 2021
$5.1M
NIEHS NIH HHS ES16893NIEHS NIH HHS R01 ES016893
6 · The paper itself

Abstract

Hexavalent chromium (Cr(VI)) compounds are known human lung carcinogens. Solubility plays an important role in its carcinogenicity with the particulate or insoluble form being the most potent. Of the particulate Cr(VI) compounds, zinc chromate appears to be the most potent carcinogen; however, very few studies have investigated its carcinogenic mechanism. In this study, we investigated the ability of chronic exposure to zinc chromate to induce numerical chromosome instability. We found no increase in aneuploidy after a 24 h exposure to zinc chromate, but with more chronic exposures, zinc chromate induced concentration- and time-dependent increases in aneuploidy in the form of hypodiploidy, hyperdiploidy, and tetraploidy. Zinc chromate also induced centrosome amplification in a concentration- and time-dependent manner in both interphase and mitotic cells after chronic exposure, producing cells with centriolar defects. Furthermore, chronic exposure to zinc chromate induced concentration- and time-dependent increases in spindle assembly checkpoint bypass with increases in centromere spreading, premature centromere division, and premature anaphase. Last, we found that chronic exposure to zinc chromate induced a G2 arrest. All together, these data indicate that zinc chromate can induce chromosome instability after prolonged exposures.

Indexed as

AneuploidyCell LineCentrosomeChromatesChromosomal InstabilityFibroblastsHumansLungParticle SizeSolubilitySpindle ApparatusZinc CompoundsChromateszinc chromateZinc Compounds

Identifiers

PMID20030412
PMCPMC2822114
OpenAlexW1969476017

What OpenQuestion holds

Textmetadata
LicenceTDM
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.