Evidence map›Paper›PMID 25485709›Full record

ArticleToxicology and applied pharmacology2015

Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure.

Wei Qu, Michael P Waalkes

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Arsenome, Arsenobolome, and Arsenobiolome.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Arsenic-induced neurotoxicity: a mechanistic appraisal.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Chronic Kidney Disease and Exposure to Nephrotoxic Metals.International journal of molecular sciences · 2017
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Wei QuNational Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Electronic address: qu@niehs.nih.gov.
Michael P WaalkesNational Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
National Institute of Environmental Health Sciences · US

Funding

Stem Cell ToxicologyZIAES102925 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TOKAR, ERIK · 2010 to 2021
$25.3M
Intramural NIH HHS ZIA ES102925NIEHS NIH HHS ES-102925
6 · The paper itself

Abstract

We studied how protein metallothionein (MT) impacts arsenic-induced oxidative DNA damage (ODD) using cells that poorly express MT (MT-I/II double knockout embryonic cells; called MT-null cells) and wild-type (WT) MT competent cells. Arsenic (as NaAsO2) was less cytolethal over 24h in WT cells (LC50=11.0±1.3μM; mean±SEM) than in MT-null cells (LC50=5.6±1.2μM). ODD was measured by the immuno-spin trapping method. Arsenic (1 or 5μM; 24h) induced much less ODD in WT cells (121% and 141% of control, respectively) than in MT-null cells (202% and 260%). In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene. In contrast, basal MT levels were not detectable in MT-null cells and unaltered by arsenic exposure. Transfection of MT-I gene into the MT-null cells markedly reduced arsenic-induced ODD levels. The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells. Arsenic caused increases in oxidant stress defense genes HO-1 and GSTα2 in both WT and MT-null cells, but to much higher levels in WT cells. WT cells appear more adept at activating metal transport systems and oxidant response genes, although the role of MT in these responses is unclear. Overall, MT protects against arsenic-induced ODD in MT competent cells by potential sequestration of scavenging oxidant radicals and/or arsenic.

Indexed as

DNA DamageAnimalsArsenicATP-Binding Cassette, Sub-Family C ProteinsCarcinogensCell LineCell ProliferationCell SurvivalDNA-Binding ProteinsEnvironmental PollutantsGene Expression RegulationGlutathione TransferaseHeme Oxygenase-1IsoenzymesMembrane ProteinsMetallothioneinArsenicATP-Binding Cassette, Sub-Family C ProteinsCarcinogensDNA-Binding ProteinsEnvironmental Pollutantsglutathione S-transferase alphaGlutathione TransferaseHeme Oxygenase-1Hmox1 protein, mouseIsoenzymesMembrane ProteinsMetallothioneinmultidrug resistance-associated protein 1Multidrug Resistance-Associated Protein 2Transcription Factor MTF-1Transcription FactorsArsenicMetallothioneinOxidative DNA damageReactive oxygen species

Identifiers

PMID25485709
PMCPMC4315697
OpenAlexW2068627337

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.