Evidence map›Paper›PMID 15309445›Full record

Trial reportEuropean journal of nutrition2004

Vitamin C supplementation decreases oxidative DNA damage in mononuclear blood cells of smokers.

Peter Møller, Michael Viscovich, Jens Lykkesfeldt, Steffen Loft, Annie Jensen, Henrik E Poulsen

Abstract readClinical TrialRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in European journal of nutrition, 2004. 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
6.1field-weighted citation impact, top 4% 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, 99 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

Peter MøllerInstitute of Public Health (c/o Dept. of Pharmacology), The Panum Institute, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen, Denmark. fipm@farmakol.ku.dk.
Michael Viscovich
Jens Lykkesfeldt
Steffen Loft
Annie Jensen
Henrik E Poulsen
University of Copenhagen · DKCopenhagen University Hospital · DKRoyal Agricultural University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntioxidants, in particular vitamin C, have been suggested to decrease oxidative DNA damage. Such effects have been shown in mononuclear blood cells in the first few hours after ingestion, whereas studies of longer-term effects in well-nourished humans have been mainly negative.

aimTo investigate the antioxidant effect of vitamin C in terms of oxidative DNA damage measured by the comet assay and DNA repair measured by expression of OGG1 mRNA in blood cells of male smokers given 2 x 250 mg vitamin C daily as plain or slow release tablets combined with plain release vitamin E 2 x 91 mg, or placebo for 4 wk.

resultsThis study showed a difference in DNA protective effects between a slow release and a plain release vitamin C formulation. Ingestion of slow release vitamin C formulation was associated with fewer endonuclease III and formamidopyrimidine DNA glycosylase sensitive sites measured by the comet assay in mononuclear blood cells obtained 4 h and 8 h after a single tablet and 4 wk after two tablets a day. Ingestion of the vitamin formulation with plain release only indicated a damage-reducing effect 4 h after intake of a single tablet, and the effect was more apparent on endonuclease III than formamidopyrimidine DNA glycosylase sites. Overall the slow release tablets of vitamin C formulation had a more pronounced and a sustained protective effect on base damage compared with the plain release tablets. Plasma vitamin E was unaltered in the first 12 h after ingestion of a single tablet, suggesting that the antioxidant effect was mediated by vitamin C. Differences in plasma vitamin C levels at steady state could not explain the difference between the two vitamin C formulations, whereas wider amplitudes of plasma vitamin C were seen after ingestion of plain release formulation compared to slow release formulation. Assessment of OGG1 mRNA levels by RT-PCR did not indicate increased expression of this DNA repair gene after 4 wk of vitamin supplementation.

conclusionThis study suggests that long-term vitamin C supplementation at high dose, i. e. 500 mg together with vitamin E in moderate dose, 182 mg, decreases the steady-state level of oxidative DNA damage in mononuclear blood cells of smokers.

Indexed as

AdultAgedAntioxidantsAscorbic AcidComet AssayDelayed-Action PreparationsDNA DamageDNA-Formamidopyrimidine GlycosylaseDNA GlycosylasesDose-Response Relationship, DrugEndonucleasesGene Expression Regulation, EnzymologicHumansLeukocytes, MononuclearMaleMiddle AgedAntioxidantsAscorbic AcidDelayed-Action PreparationsDNA-Formamidopyrimidine GlycosylaseDNA GlycosylasesEndonucleasesoxoguanine glycosylase 1, humanRNA, MessengerVitamin E

Identifiers

PMID15309445
OpenAlexW2108645163

What OpenQuestion holds

Textmetadata
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.