Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress

Fleming, Aaron M; Burrows, Cynthia J

doi:10.1093/nar/gkaf1320

Cited by 6Telomeres, Telomerase, and SenescenceDNA Repair MechanismsDNA and Nucleic Acid Chemistry

Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress

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Fleming, Aaron M, Burrows, Cynthia J·2025·Nucleic Acids Research

DOI 10.1093/nar/gkaf1320PMC PMC12684392

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Abstract

Telomere dysfunction and attrition are observed in cells subjected to oxidative or inflammatory stress, largely due to DNA damage. In this study, we applied a DNA glycosylase-assisted quantitative PCR (qPCR) assay to assess telomeric DNA damage in human cells exposed to defined sources of oxidative or inflammatory stress. As a consequence of the endogenous chemistry of these stressors being different, we were able to identify distinct types of telomere DNA damage that differentiate oxidative from inflammatory stress. By selecting lesion-specific DNA glycosylases before qPCR analysis, we determined that reactive oxygen species generated under physiological bicarbonate buffering during both oxidative and inflammatory stress primarily damaged 2′-deoxyguanosine (dG) residues. In contrast, inflammatory stress increased dG oxidation sites and nitrosative DNA damage, evidenced by deamination of 2′-deoxycytosine (dC) to 2′-deoxyuridine (dU) and 2′-deoxyadenosine (dA) to 2′-deoxyinosine (dI; hypoxanthine). During inflammation, telomeric DNA contained 1.5-fold more dU than dI. These nitrosative lesions require different DNA repair enzymes compared with dG oxidation products, and they may impact telomere structure differently. Our findings suggest that beyond dG oxidation, nitrosative DNA damage can be a major source of lesions in telomeres. The profile of telomere DNA lesions can serve as a biomarker to distinguish between oxidative and inflammatory stress.

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Oxidative and inflammatory stress can damage telomeric DNA and alter mitochondrial function, while mitochondrial reactive oxygen species may further affect telomere maintenance.
“Oxidative and inflammatory stress can damage telomeric DNA and alter mitochondrial function, while mitochondrial reactive oxygen species may further affect telomere maintenance [128,129,130].”
From Placental Pathophysiology and Developmental Programming of Adult Cardiometabolic Risk: A Narrative Review of Pregnancy Exposures (2026) · cites this paper as [130]
The Introduction reports telomeric DNA lesions under oxidative and inflammatory stress and identifies mitochondria as a major source of reactive oxygen species. It also associates oxidative stress caused by mitochondrial dysfunction with telomere attrition. It does not say that oxidative or inflammatory stress alters mitochondrial function; that reverses the relationship described. (LLM, conf=0.85)
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Telomere uncapping by common oxidative guanine lesions: Insights from atomistic models
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The origin of oxidized guanine resolves the puzzle of oxidation-induced telomere-length alterations
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Targeted DNA damage at individual telomeres disrupts their integrity and triggers cell death
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Authors: Fleming, A. M., & Burrows, C. J.
Affiliations: University of Utah (US)
Corresponding author: Fleming, Aaron M
Burrows, Cynthia J
ORCID: Fleming, Aaron M
Burrows, Cynthia J
Venue: Nucleic Acids Research
Publisher: Oxford University Press (OUP)
Published: 2025-11-26
Volume: 53
Issue: 22
ISSN: 0305-1048 (ISSN-L)
1362-4962
DOI: 10.1093/nar/gkaf1320
PMC: PMC12684392
OpenAlex: W4417183612
Cited by: 6
References: 68
Citations by year: 2026: 6
FWCI: 3.86
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor, 12 d)
Locations: Nucleic Acids Research (publishedVersion, cc-by)
PubMed (publishedVersion)
PubMed Central (publishedVersion, cc-by)
Funders: National Institutes of Health (R35 GM145237)
National Cancer Institute (P30 CA042014)
the University of Utah
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
Keywords: oxidative stress, inflammatory stress, reactive oxygen species, 2'-deoxyuridine, 2'-deoxyinosine, DNA glycosylase, DNA repair, telomere dysfunction, stress biomarkers, bicarbonate buffering
MeSH terms: Deamination, Deoxyguanosine, Deoxyribonucleosides, DNA Damage, Humans, Inflammation, Oxidation-Reduction, Polymerase Chain Reaction, Telomere, Reactive Oxygen Species, Oxidative Stress, DNA Glycosylases, HEK293 Cells, Telomere Shortening

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Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress

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