High doses of synthetic antioxidants induce premature senescence in cultivated mesenchymal stem cells
| Autor: | Olga G. Lyublinskaya, N. A. Pugovkina, Tatyana M. Grinchuk, Ju. S. Kornienko, N. N. Nikolsky, N. D. Aksenov, M. A. Shilina, Alla N. Shatrova, V. V. Zenin, Irina Smirnova, Ju. S. Ivanova |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cell cycle checkpoint Antioxidant DNA damage medicine.medical_treatment lcsh:Medicine Resveratrol medicine.disease_cause Article Antioxidants 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Humans lcsh:Science Cellular Senescence Cell Proliferation chemistry.chemical_classification Reactive oxygen species Multidisciplinary Chemistry Cell growth lcsh:R Mesenchymal stem cell Mesenchymal Stem Cells Cell Cycle Checkpoints Cell biology Oxidative Stress 030104 developmental biology lcsh:Q Female Reactive Oxygen Species 030217 neurology & neurosurgery Oxidative stress DNA Damage |
| Zdroj: | Scientific Reports Scientific Reports, Vol 9, Iss 1, Pp 1-13 (2019) |
| ISSN: | 2045-2322 |
| Popis: | Stress-induced premature senescence program is known to be activated in cells by various genotoxic stressors, and oxidative stress is considered to be the main of those. To this end, many studies discover antioxidants as protective anti-aging agents. In the current study, we examined the effects of different antioxidants (Tempol, resveratrol, NAC, DPI) on the mesenchymal stem cells maintained in normal physiological conditions. We used high, but non-cytotoxic antioxidant doses which are widely used in laboratory practice to protect cells from oxidative damage. We show that these substances induce reversible block of cell proliferation and do not cause any genotoxic effects when applied to the quiescent cells. However, the same doses of the same substances, when applied to the proliferating cells, can induce irreversible cell cycle arrest, DNA strand breaks accumulation and DNA damage response activation. As a consequence, antioxidant-induced DNA damage results in the stress-induced premature senescence program activation. We conclude that high doses of antioxidants, when applied to the proliferating cells that maintain physiological levels of reactive oxygen species, can cause DNA damage and induce premature senescence which suggests to re-estimate believed unconditional anti-aging antioxidant properties. |
| Databáze: | OpenAIRE |
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