Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation
Background: Exposure to low dose rate (LDR) radiation may accelerate aging processes. Previously, we identified numerous LDR-induced pathways involved in oxidative stress (OS) and antioxidant systems, suggesting that these pathways protect against premature senescence (PS). This study aimed to inves...
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| Format: | Article |
| Language: | English |
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IMR Press
2023-11-01
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| Series: | Frontiers in Bioscience-Landmark |
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| Online Access: | https://www.imrpress.com/journal/FBL/28/11/10.31083/j.fbl2811296 |
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| author | Traimate Sangsuwan Ali Pour Khavari Evelina Blomberg Tajanena Romell Paulo Roberto D'auria Vieira De Godoy Mats Harms-Ringdahl Siamak Haghdoost |
| author_facet | Traimate Sangsuwan Ali Pour Khavari Evelina Blomberg Tajanena Romell Paulo Roberto D'auria Vieira De Godoy Mats Harms-Ringdahl Siamak Haghdoost |
| author_sort | Traimate Sangsuwan |
| collection | DOAJ |
| description | Background: Exposure to low dose rate (LDR) radiation may accelerate aging processes. Previously, we identified numerous LDR-induced pathways involved in oxidative stress (OS) and antioxidant systems, suggesting that these pathways protect against premature senescence (PS). This study aimed to investigate if there are differences between young replicative senescent (RS) and PS cells considering DNA repair kinetics, OS, and DNA damage localized in the telomeres. Methods: We established PS cells by culturing and passaging young primary fibroblasts exposed to LDR. Then, RS cells were established by culturing and passaging young fibroblasts until they stopped proliferating. Senescence was characterized by analyzing telomere length and senescence-associated β-galactosidase (SA-β-gal) staining. DNA damage and repair were evaluated with γH2AX foci formation; telomere identification was carried out using the fluorescence in situ hybridization (FISH) probe; and oxidative stress was assessed by measuring 8-oxo-dG in the medium. Results: The data indicate the following: young cells have a better ability to cope with LDR-induced oxidative stress; RS and PS have higher steady-state levels of DNA damage; RS have slower DNA repair kinetics; and PS/RS have elevated levels of telomeric DNA damage. Conclusion: Our main conclusion is that PS and RS differ regarding DNA repair kinetics and SA-β-gal levels. |
| first_indexed | 2024-03-09T01:59:54Z |
| format | Article |
| id | doaj.art-a9b55fbed3164bf4b0beb1369eeeccfb |
| institution | Directory Open Access Journal |
| issn | 2768-6701 |
| language | English |
| last_indexed | 2024-03-09T01:59:54Z |
| publishDate | 2023-11-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Frontiers in Bioscience-Landmark |
| spelling | doaj.art-a9b55fbed3164bf4b0beb1369eeeccfb2023-12-08T07:49:20ZengIMR PressFrontiers in Bioscience-Landmark2768-67012023-11-01281129610.31083/j.fbl2811296S2768-6701(23)01046-8Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing RadiationTraimate Sangsuwan0Ali Pour Khavari1Evelina Blomberg2Tajanena Romell3Paulo Roberto D'auria Vieira De Godoy4Mats Harms-Ringdahl5Siamak Haghdoost6Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, SwedenBackground: Exposure to low dose rate (LDR) radiation may accelerate aging processes. Previously, we identified numerous LDR-induced pathways involved in oxidative stress (OS) and antioxidant systems, suggesting that these pathways protect against premature senescence (PS). This study aimed to investigate if there are differences between young replicative senescent (RS) and PS cells considering DNA repair kinetics, OS, and DNA damage localized in the telomeres. Methods: We established PS cells by culturing and passaging young primary fibroblasts exposed to LDR. Then, RS cells were established by culturing and passaging young fibroblasts until they stopped proliferating. Senescence was characterized by analyzing telomere length and senescence-associated β-galactosidase (SA-β-gal) staining. DNA damage and repair were evaluated with γH2AX foci formation; telomere identification was carried out using the fluorescence in situ hybridization (FISH) probe; and oxidative stress was assessed by measuring 8-oxo-dG in the medium. Results: The data indicate the following: young cells have a better ability to cope with LDR-induced oxidative stress; RS and PS have higher steady-state levels of DNA damage; RS have slower DNA repair kinetics; and PS/RS have elevated levels of telomeric DNA damage. Conclusion: Our main conclusion is that PS and RS differ regarding DNA repair kinetics and SA-β-gal levels.https://www.imrpress.com/journal/FBL/28/11/10.31083/j.fbl2811296radiationchronic radiationlow dose ratepremature senescencereplicative senescencedna repairradiotherapyoxidative stresshmth1telomere lengthextracellular 8-oxo-dg |
| spellingShingle | Traimate Sangsuwan Ali Pour Khavari Evelina Blomberg Tajanena Romell Paulo Roberto D'auria Vieira De Godoy Mats Harms-Ringdahl Siamak Haghdoost Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation Frontiers in Bioscience-Landmark radiation chronic radiation low dose rate premature senescence replicative senescence dna repair radiotherapy oxidative stress hmth1 telomere length extracellular 8-oxo-dg |
| title | Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation |
| title_full | Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation |
| title_fullStr | Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation |
| title_full_unstemmed | Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation |
| title_short | Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation |
| title_sort | oxidative stress levels and dna repair kinetics in senescent primary human fibroblasts exposed to chronic low dose rate of ionizing radiation |
| topic | radiation chronic radiation low dose rate premature senescence replicative senescence dna repair radiotherapy oxidative stress hmth1 telomere length extracellular 8-oxo-dg |
| url | https://www.imrpress.com/journal/FBL/28/11/10.31083/j.fbl2811296 |
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