scholarly journals DNA Repair Measured by the Comet Assay

DNA Repair ◽  
10.5772/22504 ◽  
2011 ◽  
Author(s):  
Amaya Azqueta ◽  
Sergey Shaposhnikov ◽  
Andrew R.
Keyword(s):  
2002 ◽  
Vol 128 (6) ◽  
pp. 698 ◽  
Author(s):  
David J. Terris ◽  
Edith Y. Ho ◽  
Hani Z. Ibrahim ◽  
Mary Jo Dorie ◽  
Mary S. Kovacs ◽  
...  

2019 ◽  
Vol 781 ◽  
pp. 71-87 ◽  
Author(s):  
Amaya Azqueta ◽  
Sabine A.S. Langie ◽  
Elisa Boutet-Robinet ◽  
Susan Duthie ◽  
Carina Ladeira ◽  
...  

2020 ◽  
Vol 94 (12) ◽  
pp. 4219-4228
Author(s):  
Vanessa Valdiglesias ◽  
María Sánchez-Flores ◽  
Natalia Fernández-Bertólez ◽  
William Au ◽  
Eduardo Pásaro ◽  
...  

2000 ◽  
Vol 56 (2-3) ◽  
pp. 118-131 ◽  
Author(s):  
Nathalie Rousset ◽  
Erwann Kerninon ◽  
Sabine Eléouet ◽  
Tanguy Le Néel ◽  
Jean-Louis Auget ◽  
...  

2007 ◽  
Vol 25 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Isabel Gaivão ◽  
Anita Piasek ◽  
Asgeir Brevik ◽  
Sergey Shaposhnikov ◽  
Andrew R. Collins

2014 ◽  
Vol 11 (4) ◽  
pp. 770-776 ◽  
Author(s):  
Stephanie Whisnant Cash ◽  
Shirley A.A. Beresford ◽  
Thomas L. Vaughan ◽  
Patrick J. Heagerty ◽  
Leslie Bernstein ◽  
...  

Background:Limited evidence suggests that very high-intensity exercise is positively associated with DNA damage but moderate exercise may be associated with DNA repair.Methods:Participants were 220 healthy, Washington State 50- to 76-year-olds in the validity/biomarker substudy of the VITamins And Lifestyle (VITAL) cohort, who provided blood samples and completed questionnaires assessing recent physical activity and demographic and health factors. Measures included nested activity subsets: total activity, moderate- plus high-intensity activity, and high-intensity activity. DNA damage (n = 122) and repair (n = 99) were measured using the comet assay. Multivariate linear regression was used to estimate regression coefficients and associated 95% confidence intervals (CIs) for relationships between MET-hours per week of activity and each DNA outcome (damage, and 15- and 60-minute repair capacities).Results:DNA damage was not associated with any measure of activity. However, 60-minute DNA repair was positively associated with both total activity (β = 0.21, 95% CI: 0.0057–0.412; P = .044) and high-intensity activity (β = 0.31, 95% CI: 0.20–0.60; P = .036), adjusting for age, sex, BMI, and current multivitamin use.Conclusions:This study is the first to assess broad ranges of activity intensity levels related to DNA damage and repair. Physical activity was unrelated to DNA damage but was associated with increased repair.


Blood ◽  
2002 ◽  
Vol 100 (3) ◽  
pp. 845-853 ◽  
Author(s):  
Claudia Buschfort-Papewalis ◽  
Thomas Moritz ◽  
Bernd Liedert ◽  
Jürgen Thomale

Abstract Although DNA repair processes have been shown to considerably modulate the cytotoxic effects of alkylating agents, little information is available on the role of these mechanisms in chemotherapy-induced myelosuppression. Therefore, we have analyzed in detail the DNA repair capacity of primary human hematopoietic cells from cord blood (CB) or bone marrow (BM) by 2 functional assays, the immunocytologic assay (ICA) and single-cell gel electrophoresis (comet assay). Besides substantial interindividual differences, we consistently observed significantly lower repair capacity of CD34+ cells in comparison to CD34−, CD19+, or CD33+ cells of the same donor. After exposure to the alkylating agent ethylnitrosourea (EtNU), the comet assay displayed on average twice as many DNA single-strand breaks (SSBs) in CD34+ cells and a tripled half-life of these lesions in comparison to corresponding CD34− cells. Similarly, reduced SSB repair activity in CD34+ cells was detected following melphalan or cisplatin application. When specific antibodies were used to monitor DNA reaction products of these drugs, adduct levels were significantly higher and lesions persisted longer in the CD34+ fraction. To assess the contribution of individual pathways to overall DNA repair, modulators blocking defined steps in repair processes were coapplied with alkylating drugs. Similar “modulation pattern” in corresponding CD34+ and CD34− cell fractions indicated a generalized reduction in DNA repair capacity of CD34+ cells, rather than deficiencies in a specific pathway. Because CD34+ cells also displayed higher frequencies of apoptosis in response to melphalan or cisplatin, these findings may help to explain the myelosuppression after exposure to alkylating agents.


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