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Cited by 856Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsRedox biology and oxidative stress

Mild hyperoxia shortens telomeres and inhibits proliferation of fibroblasts: a model for senescence?

von Zglinicki, Thomas, Saretzki, Gabriele, Döcke, Wolf, Lotze, Christian·1995·Experimental Cell Research
DOI 10.1006/excr.1995.1305
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Abstract

Mild oxidative stress as exerted by culture of human WI-38 fibroblasts under 40% oxygen partial pressure blocks proliferation irreversibly after one to three population doublings. Hyperoxically blocked cells are similar to senescent ones in terms of general morphology and lipofuscin accumulation. Moreover, they, like senescent fibroblasts, are blocked preferentially in G1 as evident from DNA content measurements by flow cytometry. Southern blotting of AluI- and HinfI-restricted genomic DNA shows an increase of the rate of telomere shortening from 90 bp per population doubling under normoxia to more than 500 bp per population doubling under hyperoxia. In every case, proliferation is blocked if a telomere cutoff length of about 4 kb is arrived at. The fact that telomere length correlates with the final inhibition of proliferation under conditions of varied oxidative stress, while the population doubling level does not, suggests that telomere shortening provides the signal for cell cycle exit in senescence. In postmitotic cells, no further telomere shortening occurs. However, the sensitivity of terminal restriction fragments to S1 nuclease increases, indicating the accumulation of single-strand breaks in telomeres of nondividing fibroblasts. This effect is found both under normoxic and hyperoxic culture, although it is more pronounced under conditions of higher oxidative stress. It might be speculated that accumulation of single-strand breaks and the resultant loss of distal single-stranded fragments during replication could be a major cause of telomere shortening, possibly more important than incomplete replication per se.

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Crossref · 10.1006/excr.1995.1305

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  • Mild oxidative stress accelerates telomere shortening, leading to reduced replicative capacity and a phenotype resembling replicative senescence.

    “telomere shortening is accelerated when cells are exposed to mild oxidative stress, leading to reduced replicative capacity and a phenotype that resembles replicative senescence (von Zglinicki et al., 1995, von Zglinicki, 2002, Saretzki et al., 2003).”

    From Telomeres and cell senescence—size matters not (2017) · cites this paper as von Zglinicki et al., 1995

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Authors
von Zglinicki, T., Saretzki, G., Döcke, W., & Lotze, C.
Affiliations
Humboldt-Universität zu Berlin (DE)
ORCID
Saretzki, Gabriele
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
1995-09
Volume
220
Issue
1
Pages
186-193
ISSN
0014-4827 (ISSN-L)
DOI
10.1006/excr.1995.1305
OpenAlex
W2071673220
Cited by
856
References
0
Citations by year
2026: 5 · 2025: 12 · 2024: 12 · 2023: 15 · 2022: 23 · 2021: 27 · 2020: 18 · 2019: 27 · 2018: 16 · 2017: 19 · 2016: 23 · 2015: 27 · 2014: 26 · 2013: 28 · 2012: 34
FWCI
8.20
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Cell Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
hyperoxia, telomere shortening, cellular senescence, fibroblast proliferation, oxidative stress, WI-38 cells, G1 cell cycle arrest, telomere length, terminal restriction fragments, S1 nuclease, lipofuscin, postmitotic cells
MeSH terms
Aerobiosis, Cell Cycle, Cells, Cultured, Fibroblasts, Flow Cytometry, Lipofuscin, Microscopy, Electron, Oxygen, Phenotype, Ploidies, Oligonucleotide Probes, Telomere, Cellular Senescence, Oxidative Stress

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