Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest

Many environmental and physiological stresses are chronic. Thus, cells are constantly exposed to diverse types of genotoxic insults that challenge genome stability, including those that induce oxidative DNA damage. However, most in vitro studies that model cellular response to oxidative stressors em...

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Autores Principales: Santa-Gonzalez, Gloria A., Gomez-Molina, Andrea, Arcos-Burgos, Mauricio, Meyer, Joel N., Camargo, Mauricio
Formato: Artículo (Article)
Lenguaje:Inglés (English)
Publicado: Elsevier 2016
Materias:
ROS
Acceso en línea:https://repository.urosario.edu.co/handle/10336/27532
https://doi.org/10.1016/j.redox.2016.07.004
id ir-10336-27532
recordtype dspace
spelling ir-10336-275322021-01-21T08:06:06Z Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest Respuesta adaptativa distintiva a la exposición repetida al peróxido de hidrógeno asociada con la regulación positiva de los genes de reparación del ADN y la detención del ciclo celular Santa-Gonzalez, Gloria A. Gomez-Molina, Andrea Arcos-Burgos, Mauricio Meyer, Joel N. Camargo, Mauricio ROS Genotoxicity DNA damage response Up-regulation of DNA repair genes G2/M arrest Adaptation Many environmental and physiological stresses are chronic. Thus, cells are constantly exposed to diverse types of genotoxic insults that challenge genome stability, including those that induce oxidative DNA damage. However, most in vitro studies that model cellular response to oxidative stressors employ short exposures and/or acute stress models. In this study, we tested the hypothesis that chronic and repeated exposure to a micromolar concentration of hydrogen peroxide (H2O2) could activate DNA damage responses, resulting in cellular adaptations. For this purpose, we developed an in vitro model in which we incubated mouse myoblast cells with a steady concentration of ~50 ?M H2O2 for one hour daily for seven days, followed by a final challenge of a 10 or 20X higher dose of H2O2 (0.5 or 1 mM). We report that intermittent long-term exposure to this oxidative stimulus nearly eliminated cell toxicity and significantly decreased genotoxicity (in particular, a >5-fold decreased in double-strand breaks) resulting from subsequent acute exposure to oxidative stress. This protection was associated with cell cycle arrest in G2/M and induction of expression of nine DNA repair genes. Together, this evidence supports an adaptive response to chronic, low-level oxidative stress that results in genomic protection and up-regulated maintenance of cellular homeostasis. 2016-10 2020-08-19T14:42:36Z info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion ISSN: 2213-2317 https://repository.urosario.edu.co/handle/10336/27532 https://doi.org/10.1016/j.redox.2016.07.004 eng info:eu-repo/semantics/openAccess application/pdf Elsevier Redox Biology
institution EdocUR - Universidad del Rosario
collection DSpace
language Inglés (English)
topic ROS
Genotoxicity
DNA damage response
Up-regulation of DNA repair genes
G2/M arrest
Adaptation
spellingShingle ROS
Genotoxicity
DNA damage response
Up-regulation of DNA repair genes
G2/M arrest
Adaptation
Santa-Gonzalez, Gloria A.
Gomez-Molina, Andrea
Arcos-Burgos, Mauricio
Meyer, Joel N.
Camargo, Mauricio
Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
description Many environmental and physiological stresses are chronic. Thus, cells are constantly exposed to diverse types of genotoxic insults that challenge genome stability, including those that induce oxidative DNA damage. However, most in vitro studies that model cellular response to oxidative stressors employ short exposures and/or acute stress models. In this study, we tested the hypothesis that chronic and repeated exposure to a micromolar concentration of hydrogen peroxide (H2O2) could activate DNA damage responses, resulting in cellular adaptations. For this purpose, we developed an in vitro model in which we incubated mouse myoblast cells with a steady concentration of ~50 ?M H2O2 for one hour daily for seven days, followed by a final challenge of a 10 or 20X higher dose of H2O2 (0.5 or 1 mM). We report that intermittent long-term exposure to this oxidative stimulus nearly eliminated cell toxicity and significantly decreased genotoxicity (in particular, a >5-fold decreased in double-strand breaks) resulting from subsequent acute exposure to oxidative stress. This protection was associated with cell cycle arrest in G2/M and induction of expression of nine DNA repair genes. Together, this evidence supports an adaptive response to chronic, low-level oxidative stress that results in genomic protection and up-regulated maintenance of cellular homeostasis.
format Artículo (Article)
author Santa-Gonzalez, Gloria A.
Gomez-Molina, Andrea
Arcos-Burgos, Mauricio
Meyer, Joel N.
Camargo, Mauricio
author_facet Santa-Gonzalez, Gloria A.
Gomez-Molina, Andrea
Arcos-Burgos, Mauricio
Meyer, Joel N.
Camargo, Mauricio
author_sort Santa-Gonzalez, Gloria A.
title Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
title_short Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
title_full Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
title_fullStr Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
title_full_unstemmed Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest
title_sort distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of dna repair genes and cell cycle arrest
publisher Elsevier
publishDate 2016
url https://repository.urosario.edu.co/handle/10336/27532
https://doi.org/10.1016/j.redox.2016.07.004
_version_ 1689943200912900096
score 12,131701