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Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()

Hydrogen peroxide emerged as major redox metabolite operative in redox sensing, signaling and redox regulation. Generation, transport and capture of H(2)O(2) in biological settings as well as their biological consequences can now be addressed. The present overview focuses on recent progress on metab...

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Detalles Bibliográficos
Autor principal: Sies, Helmut
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5256672/
https://www.ncbi.nlm.nih.gov/pubmed/28110218
http://dx.doi.org/10.1016/j.redox.2016.12.035
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author Sies, Helmut
author_facet Sies, Helmut
author_sort Sies, Helmut
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description Hydrogen peroxide emerged as major redox metabolite operative in redox sensing, signaling and redox regulation. Generation, transport and capture of H(2)O(2) in biological settings as well as their biological consequences can now be addressed. The present overview focuses on recent progress on metabolic sources and sinks of H(2)O(2) and on the role of H(2)O(2) in redox signaling under physiological conditions (1–10 nM), denoted as oxidative eustress. Higher concentrations lead to adaptive stress responses via master switches such as Nrf2/Keap1 or NF-κB. Supraphysiological concentrations of H(2)O(2) (>100 nM) lead to damage of biomolecules, denoted as oxidative distress. Three questions are addressed: How can H(2)O(2) be assayed in the biological setting? What are the metabolic sources and sinks of H(2)O(2)? What is the role of H(2)O(2) in redox signaling and oxidative stress?
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spelling pubmed-52566722017-01-30 Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress() Sies, Helmut Redox Biol Review Article Hydrogen peroxide emerged as major redox metabolite operative in redox sensing, signaling and redox regulation. Generation, transport and capture of H(2)O(2) in biological settings as well as their biological consequences can now be addressed. The present overview focuses on recent progress on metabolic sources and sinks of H(2)O(2) and on the role of H(2)O(2) in redox signaling under physiological conditions (1–10 nM), denoted as oxidative eustress. Higher concentrations lead to adaptive stress responses via master switches such as Nrf2/Keap1 or NF-κB. Supraphysiological concentrations of H(2)O(2) (>100 nM) lead to damage of biomolecules, denoted as oxidative distress. Three questions are addressed: How can H(2)O(2) be assayed in the biological setting? What are the metabolic sources and sinks of H(2)O(2)? What is the role of H(2)O(2) in redox signaling and oxidative stress? Elsevier 2017-01-05 /pmc/articles/PMC5256672/ /pubmed/28110218 http://dx.doi.org/10.1016/j.redox.2016.12.035 Text en © 2017 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review Article
Sies, Helmut
Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title_full Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title_fullStr Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title_full_unstemmed Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title_short Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress()
title_sort hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: oxidative eustress()
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5256672/
https://www.ncbi.nlm.nih.gov/pubmed/28110218
http://dx.doi.org/10.1016/j.redox.2016.12.035
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