Evidence map›Paper›PMID 17431482›Full record

ArticleEnvironmental health perspectives2007

Impact of trivalent arsenicals on selenoprotein synthesis.

Denis Ganyc, Sarah Talbot, Fanta Konate, Sarah Jackson, Brian Schanen, William Cullen, William T Self

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2007. 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
3.1field-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

18 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Arsenic exposure and increasedRedox biochemistry and chemistry · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Denis GanycDepartment of Molecular Biology and Microbiology, Burnett College of Biomedical Science, University of Central Florida, Orlando, Florida 32816-2364, USA.
Sarah Talbot
Fanta Konate
Sarah Jackson
Brian Schanen
William Cullen
William T Self
University of Central Florida · USUniversity of British Columbia · CA

Funding

Impact of Arsenicals on Selenoprotein SynthesisR15ES014354 · NIEHS · UNIVERSITY OF CENTRAL FLORIDA · PI SELF, WILLIAM T · 2006 to 2006
$213k
NIEHS NIH HHS R15 ES014354
6 · The paper itself

Abstract

backgroundExposure to arsenic has been associated with development of skin, lung, bladder, liver, and kidney cancer. Recent evidence suggests that an increase in oxidative stress in cells treated with arsenicals represents the molecular mechanism behind arsenic-induced carcinogenesis. Selenium, in the form of selenocysteine, is necessary for the activity of several enzymes with a role in defense against reactive oxygen species. A mutual sparing effect between arsenic and selenium has been shown in animal studies when both metalloids are present in high concentrations.

objectivesTo determine whether changes in selenoprotein synthesis may be an underlying mechanism behind arsenic-induced carcinogenesis, we analyzed the new synthesis of selenoproteins within cells after exposure to inorganic or methylated arsenicals using a human keratinocyte cell model.

resultsAddition of arsenite to culture medium blocked new synthesis of selenoproteins when selenium was present in the form of selenite, and appeared to stimulate the use of serum-derived selenium. Monomethylarsonous acid (MMA(III)) treatment of cells, in contrast, did not block all new synthesis of selenoproteins but did result in an increase in cytosolic thioredoxin reductase (TrxR1) at both the mRNA and protein levels. MMA(III) also reduced the new synthesis of cellular glutatione peroxidase (cGpx) and other smaller selenoproteins. Dimethylarsinous acid (DMA(III)) stimulated selenoprotein synthesis by an as yet unknown mechanism.

conclusionsThese results suggest that arsenite and MMA(III) are key metabolites that trigger higher levels of TrxR1, and both lead to a reduction in the expression of cGpx. Together these effects certainly could lead to carcinogenesis given the knowledge that many cancers have higher levels of TrxR, and reduced Gpx levels will reduce the cell's ability to defend against reactive oxygen species. Based on these results, the impact of the trivalent arsenicals arsenite and MMA(III) on selenoprotein synthesis may indeed represent a potential molecular mechanism for the higher rates of cancer observed in populations exposed to high levels of arsenic.

Indexed as

AnimalsArsenicalsCell LineCell SurvivalChlorocebus aethiopsGenes, ReporterGlutathione PeroxidaseHumansKeratinocytesMiceRNA, MessengerSelenoproteinsThioredoxin-Disulfide ReductaseThioredoxin Reductase 1ArsenicalsGlutathione PeroxidaseRNA, MessengerSelenoproteinsThioredoxin-Disulfide ReductaseThioredoxin Reductase 1TXNRD1 protein, humanTxnrd1 protein, mouse

Identifiers

PMID17431482
PMCPMC1849912
OpenAlexW1991291620

What OpenQuestion holds

Textmetadata
LicenceCC0
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.