Evidence map›Paper›PMID 25462065›Full record

ArticleRedox biology2014

Role of H2O2 in the oxidative effects of zinc exposure in human airway epithelial cells.

Phillip A Wages, Robert Silbajoris, Adam Speen, Luisa Brighton, Andres Henriquez, Haiyan Tong, Philip A Bromberg, Steven O Simmons, James M Samet

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Expression of the HAntioxidants (Basel, Switzerland) · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Through the Looking Glass:Applied in vitro toxicology · 2018
    Review
  10. Article
  11. Oxidative Stress from Environmental Exposures.Current opinion in toxicology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

9 authors at 2 institutions in 1 country.

Phillip A WagesCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Robert SilbajorisEPHD, NHEERL, US Environmental Protection Agency, Chapel Hill, NC, USA.
Adam SpeenCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Luisa BrightonCEMALB, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Andres HenriquezCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Haiyan TongEPHD, NHEERL, US Environmental Protection Agency, Chapel Hill, NC, USA.
Philip A BrombergCEMALB, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Steven O SimmonsISTD, NHEERL, US Environmental Protection Agency, RTP, NC, USA.
James M SametEPHD, NHEERL, US Environmental Protection Agency, Chapel Hill, NC, USA. Electronic address: Samet.James@epa.gov.
University of North Carolina at Chapel Hill · USEnvironmental Protection Agency · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
NIEHS NIH HHS T32 ES007126NIEHS NIH HHS T32ES007126
6 · The paper itself

Abstract

Human exposure to particulate matter (PM) is a global environmental health concern. Zinc (Zn(2+)) is a ubiquitous respiratory toxicant that has been associated with PM health effects. However, the molecular mechanism of Zn(2+) toxicity is not fully understood. H2O2 and Zn(2+) have been shown to mediate signaling leading to adverse cellular responses in the lung and we have previously demonstrated Zn(2+) to cause cellular H2O2 production. To determine the role of Zn(2+)-induced H2O2 production in the human airway epithelial cell response to Zn(2+) exposure. BEAS-2B cells expressing the redox-sensitive fluorogenic sensors HyPer (H2O2) or roGFP2 (EGSH) in the cytosol or mitochondria were exposed to 50µM Zn(2+) for 5min in the presence of 1µM of the zinc ionophore pyrithione. Intracellular H2O2 levels were modulated using catalase expression either targeted to the cytosol or ectopically to the mitochondria. HO-1 mRNA expression was measured as a downstream marker of response to oxidative stress induced by Zn(2+) exposure. Both cytosolic catalase overexpression and ectopic catalase expression in mitochondria were effective in ablating Zn(2+)-induced elevations in H2O2. Compartment-directed catalase expression blunted Zn(2+)-induced elevations in cytosolic EGSH and the increased expression of HO-1 mRNA levels. Zn(2+) leads to multiple oxidative effects that are exerted through H2O2-dependent and independent mechanisms.

Indexed as

Oxidative StressAdaptation, BiologicalCatalaseGene Expression RegulationGlutathioneHeme Oxygenase-1HumansHydrogen PeroxideRespiratory MucosaZincCatalaseGlutathioneHeme Oxygenase-1Hydrogen PeroxideZincCatalaseGenetically encoded redox probesH(2)O(2)Live cell imagingMitochondriaZinc

Identifiers

PMID25462065
PMCPMC4297933
OpenAlexW2002132602

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.