Preferential Accumulation of Single-Stranded Regions in Telomeres of Human Fibroblasts
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We have demonstrated recently that chronic hyperoxic treatment accelerates the rate of aging of fibroblasts and the rate of telomere shortening in parallel. It was hypothesized that accelerated telomere shortening is due to preferential accumulation of oxidative damage in telomeres. To test this hypothesis, we measured the accumulation of sites sensitive to S1 nuclease treatment in telomeres, in minisatellites, and in the bulk of the genome of fibroblasts under different models of oxidative stress as well as after treatment with the alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine. A comparison with qualitative data obtained by alkaline electrophoresis reveals that the sites transferred to double-strand breaks by treatment with low concentrations of S1 nuclease are, in fact, single-stranded regions in the DNA. These regions may resemble single-stranded overhangs, gaps, or conventional single-strand breaks. The frequency of single-stranded regions is significantly higher in telomeres than in minisatellites or in the bulk of the genome under all conditions tested. Those regions induced in minisatellites or in the overall genome by a bolus dose of hydrogen peroxide are completely repaired within 24 h. On the other hand, 50 +/- 12% of H2O2-induced single-stranded regions remain unrepaired for at least 19 days in telomeres of human fibroblasts, leading to a significant increase of the telomeric steady-state level of these lesions. This preferential accumulation might significantly contribute to telomere shortening.
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Telomere DNA is particularly sensitive to oxidative damage, and single-strand breaks or other stress-induced lesions at telomeres are inefficiently repaired.
“As telomere DNA is particularly sensitive to oxidative damage (Oikawa & Kawanishi, 1999) and single‐strand breaks or other stress‐induced lesions at telomeres are inefficiently repaired (Petersen et al., 1998)”
From P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan (2016) · cites this paper as Petersen et al., 1998
Single-stranded breaks preferentially accumulate at telomeres under mild oxidative stress, leading to replication fork stalling, incomplete replication of chromosome ends, and accelerated telomere shortening.
“single-stranded breaks have been shown to preferentially accumulate at telomeres in conditions of mild oxidative stress, and such lesions lead to replication fork stalling, resulting in incomplete replication of chromosome ends and thus accelerated telomere shortening (Petersen et al., 1998, von Zglinicki, 2000).”
From Telomeres and cell senescence—size matters not (2017) · cites this paper as Petersen et al., 1998
Many studies associate the presence of a great amount of mitochondrial ROS with accumulated single-strand breaks in telomere regions, thus accelerating telomere erosion and cellular senescence.
“Many studies associate the presence of a great amount of mitochondrial ROS with accumulated single-strand breaks in telomere regions, thus accelerating telomere erosion and cellular senescence [106,107].”
From Role of Age-Related Mitochondrial Dysfunction in Sarcopenia (2020) · cites this paper as [106]
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- Authors
- Petersen, S., Saretzki, G., & Zglinicki, T. V.
- Affiliations
- Humboldt-Universität zu Berlin (DE)
- Corresponding author
- Zglinicki, Thomas von
- Venue
- Experimental Cell Research
- Publisher
- Elsevier BV
- Published
- 1998-02
- Volume
- 239
- Issue
- 1
- Pages
- 152-160
- ISSN
- 0014-4827 (ISSN-L)
- OpenAlex
- W2037480531
- Cited by
- 427
- References
- 33
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 9 · 2023: 17 · 2022: 15 · 2021: 14 · 2020: 14 · 2019: 19 · 2018: 18 · 2017: 14 · 2016: 23 · 2015: 15 · 2014: 16 · 2013: 17 · 2012: 20
- FWCI
- 7.99
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Experimental Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- 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 › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- telomeres, telomere shortening, oxidative DNA damage, hydrogen peroxide, S1 nuclease, minisatellites, N-methyl-N'-nitro-N-nitrosoguanidine, alkylating agents, DNA repair, human fibroblasts, hyperoxia, aging
- MeSH terms
- Cell Line, DNA, Fibroblasts, Humans, Methylnitronitrosoguanidine, Single-Strand Specific DNA and RNA Endonucleases, Telomere, Minisatellite Repeats
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