Evidence map›Paper›PMID 25354277›Full record

ArticlePloS one2014

Oxidative stress induces persistent telomeric DNA damage responsible for nuclear morphology change in mammalian cells.

Elisa Coluzzi, Monica Colamartino, Renata Cozzi, Stefano Leone, Carlo Meneghini, Nathan O'Callaghan, Antonella Sgura

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 188 citations in OpenAlex.

  1. Placental Pathophysiology and Developmental Programming of Adult Cardiometabolic Risk: A Narrative Review of Pregnancy Exposures.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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  8. Prolonged exposure to leisure screen time notably accelerates biological aging: Evidence from observational studies and genetic associations.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Observational
  9. Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025
    Review
  10. Article
  11. Article
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  13. Review
  14. Review
  15. Review
  16. Article
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39 more citing papers are in PubMed but not listed here.

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.

Elisa ColuzziDepartment of Science, University of "Roma Tre", Rome, Italy.
Monica ColamartinoDepartment of Science, University of "Roma Tre", Rome, Italy.
Renata CozziDepartment of Science, University of "Roma Tre", Rome, Italy.
Stefano LeoneDepartment of Science, University of "Roma Tre", Rome, Italy.
Carlo MeneghiniDepartment of Science, University of "Roma Tre", Rome, Italy.
Nathan O'CallaghanCSIRO Food and nutritional Sciences, Nutritional Genomics Laboratory, Adelaide, Australia.
Antonella SguraDepartment of Science, University of "Roma Tre", Rome, Italy.
Roma Tre University · ITHealth Sciences and Nutrition · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One main function of telomeres is to maintain chromosome and genome stability. The rate of telomere shortening can be accelerated significantly by chemical and physical environmental agents. Reactive oxygen species are a source of oxidative stress and can produce modified bases (mainly 8-oxoG) and single strand breaks anywhere in the genome. The high incidence of guanine residues in telomeric DNA sequences makes the telomere a preferred target for oxidative damage. Our aim in this work is to evaluate whether chromosome instability induced by oxidative stress is related specifically to telomeric damage. We treated human primary fibroblasts (MRC-5) in vitro with hydrogen peroxide (100 and 200 µM) for 1 hr and collected data at several time points. To evaluate the persistence of oxidative stress-induced DNA damage up to 24 hrs after treatment, we analysed telomeric and genomic oxidative damage by qPCR and a modified comet assay, respectively. The results demonstrate that the genomic damage is completely repaired, while the telomeric oxidative damage persists. The analysis of telomere length reveals a significant telomere shortening 48 hrs after treatment, leading us to hypothesise that residual telomere damage could be responsible for the telomere shortening observed. Considering the influence of telomere length modulation on genomic stability, we quantified abnormal nuclear morphologies (Nucleoplasmic Bridges, Nuclear Buds and Micronuclei) and observed an increase of chromosome instability in the same time frame as telomere shortening. At subsequent times (72 and 96 hrs), we observed a restoration of telomere length and a reduction of chromosome instability, leaving us to conjecture a correlation between telomere shortening/dysfunction and chromosome instability. We can conclude that oxidative base damage leads to abnormal nuclear morphologies and that telomere dysfunction is an important contributor to this effect.

Indexed as

DNA DamageOxidative StressTelomere ShorteningCell LineCell NucleusChromosomal InstabilityHumansHydrogen PeroxideTelomereHydrogen Peroxide

Identifiers

PMID25354277
PMCPMC4212976
OpenAlexW2035144476

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.