PMID- 38062840
OWN - NLM
STAT- MEDLINE
DCOM- 20231216
LR  - 20240220
IS  - 2768-6698 (Electronic)
IS  - 2768-6698 (Linking)
VI  - 28
IP  - 11
DP  - 2023 Nov 24
TI  - Oxidative Stress Levels and DNA Repair Kinetics in Senescent Primary Human 
      Fibroblasts Exposed to Chronic Low Dose Rate of Ionizing Radiation.
PG  - 296
LID - 10.31083/j.fbl2811296 [doi]
AB  - 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 
      beta-galactosidase (SA-beta-gal) staining. DNA damage and repair were evaluated with 
      gammaH2AX 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-beta-gal levels.
CI  - (c) 2023 The Author(s). Published by IMR Press.
FAU - Sangsuwan, Traimate
AU  - Sangsuwan T
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Pour Khavari, Ali
AU  - Pour Khavari A
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Blomberg, Evelina
AU  - Blomberg E
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Romell, Tajanena
AU  - Romell T
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Godoy, Paulo Roberto D'auria Vieira De
AU  - Godoy PRDV
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Harms-Ringdahl, Mats
AU  - Harms-Ringdahl M
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
FAU - Haghdoost, Siamak
AU  - Haghdoost S
AD  - Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm 
      University, SE-10691 Stockholm, Sweden.
AD  - CIMAP/ARIA team, University of Caen Normandy, 14000 Caen, France.
AD  - Advanced Resource Center for HADrontherapy in Europe (ARCHADE), 14000 Caen, 
      France.
LA  - eng
GR  - The Swedish Radiation Safety Authority, SSM/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Singapore
TA  - Front Biosci (Landmark Ed)
JT  - Frontiers in bioscience (Landmark edition)
JID - 101612996
SB  - IM
MH  - Humans
MH  - *Cellular Senescence/genetics
MH  - In Situ Hybridization, Fluorescence
MH  - *Oxidative Stress
MH  - DNA Damage
MH  - Telomere/genetics
MH  - Fibroblasts/metabolism
MH  - DNA Repair
MH  - Radiation, Ionizing
OTO - NOTNLM
OT  - DNA repair
OT  - chronic radiation
OT  - extracellular 8-oxo-dG
OT  - hMTH1
OT  - low dose rate
OT  - oxidative stress
OT  - premature senescence
OT  - radiation
OT  - radiotherapy
OT  - replicative senescence
OT  - telomere length
COIS- The authors declare no conflicts of interest.
EDAT- 2023/12/08 06:41
MHDA- 2023/12/17 13:19
CRDT- 2023/12/08 03:43
PHST- 2023/06/15 00:00 [received]
PHST- 2023/09/09 00:00 [revised]
PHST- 2023/09/13 00:00 [accepted]
PHST- 2023/12/17 13:19 [medline]
PHST- 2023/12/08 06:41 [pubmed]
PHST- 2023/12/08 03:43 [entrez]
AID - S2768-6701(23)01046-8 [pii]
AID - 10.31083/j.fbl2811296 [doi]
PST - ppublish
SO  - Front Biosci (Landmark Ed). 2023 Nov 24;28(11):296. doi: 10.31083/j.fbl2811296.