Evidence map›Paper›PMID 27015367›Full record

ArticleOncotarget2016

Oxidative stress at low levels can induce clustered DNA lesions leading to NHEJ mediated mutations.

Vyom Sharma, Leonard B Collins, Ting-Huei Chen, Natalie Herr, Shunichi Takeda, Wei Sun, James A Swenberg, Jun Nakamura

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
5.7field-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

92 citing papers in PubMed, 151 citations in OpenAlex.

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  14. Airborne PMInternational journal of molecular sciences · 2025
    Article
  15. Effects ofArhiv za higijenu rada i toksikologiju · 2025
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32 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

8 authors at 2 institutions in 2 countries.

Vyom SharmaDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, Chapel Hill, NC 27599, USA.
Leonard B CollinsDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, Chapel Hill, NC 27599, USA.
Ting-Huei ChenDepartment of Genetics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Natalie HerrDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, Chapel Hill, NC 27599, USA.
Shunichi TakedaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto 606-8501, Japan.
Wei SunDepartment of Genetics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
James A SwenbergDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, Chapel Hill, NC 27599, USA.
Jun NakamuraDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, Chapel Hill, NC 27599, USA.
University of North Carolina at Chapel Hill · USKyoto University · JP

Funding

STOCHASTIC ANALYSIS OF FLOW AND TRANSPORT PHENOMENAP42ES005948 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FRY, REBECCA · 1992 to 2017
$45.4M
UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
NIEHS NIH HHS P30 ES010126NIEHS NIH HHS P42 ES005948
6 · The paper itself

Abstract

DNA damage and mutations induced by oxidative stress are associated with various different human pathologies including cancer. The facts that most human tumors are characterized by large genome rearrangements and glutathione depletion in mice results in deletions in DNA suggest that reactive oxygen species (ROS) may cause gene and chromosome mutations through DNA double strand breaks (DSBs). However, the generation of DSBs at low levels of ROS is still controversial. In the present study, we show that H2O2 at biologically-relevant levels causes a marked increase in oxidative clustered DNA lesions (OCDLs) with a significant elevation of replication-independent DSBs. Although it is frequently reported that OCDLs are fingerprint of high-energy IR, our results indicate for the first time that H2O2, even at low levels, can also cause OCDLs leading to DSBs specifically in G1 cells. Furthermore, a reverse genetic approach revealed a significant contribution of the non-homologous end joining (NHEJ) pathway in H2O2-induced DNA repair & mutagenesis. This genomic instability induced by low levels of ROS may be involved in spontaneous mutagenesis and the etiology of a wide variety of human diseases like chronic inflammation-related disorders, carcinogenesis, neuro-degeneration and aging.

Indexed as

AnimalsCell LineChickensDNA DamageDNA End-Joining RepairHydrogen PeroxideMutagenesisOxidantsOxidative StressHydrogen PeroxideOxidantsclustered DNA lesionsdouble strand breaksmutationsNHEJoxidative stress

Identifiers

PMID27015367
PMCPMC5041911
OpenAlexW2337885453

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.