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

G.A. Santa-Gonzalez, A. Gomez-Molina, M. Arcos-Burgos, J.N. Meyer, M. Camargo

Resultado de la investigación: Contribución a RevistaArtículo

16 Citas (Scopus)

Resumen

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 μM 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 The Authors
Idioma originalEnglish (US)
Páginas (desde-hasta)124-133
Número de páginas10
PublicaciónRedox Biology
Volumen9
DOI
EstadoPublished - 2016

Huella dactilar

Cell Cycle Checkpoints
DNA Repair
Hydrogen Peroxide
Repair
Oxidative stress
Up-Regulation
Genes
Cells
DNA Damage
DNA
Oxidative Stress
G2 Phase Cell Cycle Checkpoints
Physiological Stress
Myoblasts
Genomic Instability
Toxicity
Homeostasis
Maintenance
In Vitro Techniques

Citar esto

Santa-Gonzalez, G.A. ; Gomez-Molina, A. ; Arcos-Burgos, M. ; Meyer, J.N. ; Camargo, M. / Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest. En: Redox Biology. 2016 ; Vol. 9. pp. 124-133.
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Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest. / Santa-Gonzalez, G.A.; Gomez-Molina, A.; Arcos-Burgos, M.; Meyer, J.N.; Camargo, M.

En: Redox Biology, Vol. 9, 2016, p. 124-133.

Resultado de la investigación: Contribución a RevistaArtículo

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T1 - Distinctive adaptive response to repeated exposure to hydrogen peroxide associated with upregulation of DNA repair genes and cell cycle arrest

AU - Santa-Gonzalez, G.A.

AU - Gomez-Molina, A.

AU - Arcos-Burgos, M.

AU - Meyer, J.N.

AU - Camargo, M.

N1 - Cited By :8 Export Date: 4 April 2018

PY - 2016

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N2 - 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 μM 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 The Authors

AB - 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 μM 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 The Authors

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