H2O2 is operative in redox sensing and redox signaling.
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H2O2 reacts with metal centers and with sulfur/selenium compounds.
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H2O2 links redox biology to phosphorylation/dephosphorylation.
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Physiological (low-level, nM) steady-state of H2O2 is maintained in oxidative eustress.
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Supraphysiological (pathological) level of H2O2 leads to oxidative distress.
Abstract
Hydrogen peroxide emerged as major redox metabolite operative in redox sensing, signaling and redox regulation. Generation, transport and capture of H2O2 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 H2O2 and on the role of H2O2 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 H2O2 (>100 nM) lead to damage of biomolecules, denoted as oxidative distress. Three questions are addressed: How can H2O2 be assayed in the biological setting? What are the metabolic sources and sinks of H2O2? What is the role of H2O2 in redox signaling and oxidative stress?
This article is based, in part, on a lecture entitled “Oxidative Stress and Redox Signaling: Role of Hydrogen Peroxide”, which was presented at the XI Reunion del Grupo Espanol de Investigacion en Radicales Libres (GEIRLI), September 13, 2016, at Granada, Spain.
