Evidence map›Paper›PMID 26658762›Full record

ArticleEuropean journal of nutrition2016

DNA damage and oxidative stress response to selenium yeast in the non-smoking individuals: a short-term supplementation trial with respect to GPX1 and SEPP1 polymorphism.

E Jablonska, S Raimondi, J Gromadzinska, E Reszka, E Wieczorek, M B Krol, A Smok-Pieniazek, M Nocun, M Stepnik, K Socha and 2 more

Open access · hybridAbstract read
In one paragraph

Article in European journal of nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Selenium for preventing cancer.The Cochrane database of systematic reviews · 2018
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Oxidative stress and prostatic diseases.Molecular and clinical oncology · 2017
    Article
  6. 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

12 authors at 3 institutions in 2 countries.

E JablonskaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland. ewa@imp.lodz.pl.
S RaimondiDivision of Epidemiology and Biostatistics, European Institute of Oncology, Via Ripamonti 435, Milan, Italy.
J GromadzinskaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
E ReszkaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
E WieczorekDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
M B KrolDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
A Smok-PieniazekDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
M NocunDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
M StepnikDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
K SochaDepartment of Bromatology, Medical University of Bialystok, Mickiewicza 2D Street, 15-222, Białystok, Poland.
M H BorawskaDepartment of Bromatology, Medical University of Bialystok, Mickiewicza 2D Street, 15-222, Białystok, Poland.
W WasowiczDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, St. Teresy 8 Street, 91-348, Lodz, Poland.
Nofer Institute of Occupational Medicine · PLMedical University of Białystok · PLEuropean Institute of Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSelenium, both essential and toxic element, is considered to protect against cancer, though human supplementation trials have generated many inconsistent data. Genetic background may partially explain a great variability of the studies related to selenium and human health. The aim of this study was to assess whether functional polymorphisms within two selenoprotein-encoding genes modify the response to selenium at the level of oxidative stress, DNA damage, and mRNA expression, especially in the individuals with a relatively low selenium status.

methodsThe trial involved 95 non-smoking individuals, stratified according to GPX1 rs1050450 and SEPP1 rs3877899 genotypes, and supplemented with selenium yeast (200 µg) for 6 weeks. Blood was collected at four time points, including 4 weeks of washout.

resultsAfter genotype stratification, the effect of GPX1 rs1050450 on lower GPx1 activity responsiveness was confirmed; however, in terms of DNA damage, we failed to indicate that individuals homozygous for variant allele may especially benefit from the increased selenium intake. Surprisingly, considering gene and time interaction, GPX1 polymorphism was observed to modify the level of DNA strand breaks during washout, showing a significant increase in GPX1 wild-type homozygotes. Regardless of the genotype, selenium supplementation was associated with a selectively suppressed selenoprotein mRNA expression and inconsistent changes in oxidative stress response, indicating for overlapped, antioxidant, and prooxidant effects. Intriguingly, DNA damage was not influenced by supplementation, but it was significantly increased during washout.

conclusionsThese results point to an unclear relationship between selenium, genotype, and DNA damage.

Indexed as

Dietary SupplementsAdolescentAdultAllelesBody Mass IndexDNA DamageFemaleGenotypeGenotyping TechniquesGlutathione PeroxidaseGlutathione Peroxidase GPX1HumansLipid PeroxidationMaleMiddle AgedOxidative StressGlutathione PeroxidaseGlutathione Peroxidase GPX1RNA, MessengerSeleniumSelenoproteinsDNA damageGene expressionOxidative stressSeleniumSelenium supplementationSelenoproteins

Identifiers

PMID26658762
PMCPMC5122617
OpenAlexW2296262059

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.