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 (1–10nM), 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 (>100nM) 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?
Highlights
(or unsurprisingly, in hindsight) hydrogen peroxide emerged as the major redox metabolite operative in redox sensing, signaling and redox regulation·H2O2 is recognized as being in the forefront of transcription-independent signal molecules, in one line with Ca2+ and ATP [2,3]
It became clear that H2O2 serves fundamental regulatory functions in metabolism beyond the role as damage signal [4]
The metabolic and regulatory role of this oxygen metabolite has been increasingly recognized [5]. It serves as a key molecule in the Third Principle of the Redox Code, which is: “Redox sensing through activation/deactivation cycles of H2O2 production linked to the NAD and NADP systems to support spatiotemporal organisation of key processes” [6]·H2O2 occurs in normal metabolism in mammalian cells [7] and is a key metabolite in oxidative stress
Summary
(or unsurprisingly, in hindsight) hydrogen peroxide emerged as the major redox metabolite operative in redox sensing, signaling and redox regulation (see [1] for recent review)·H2O2 is recognized as being in the forefront of transcription-independent signal molecules, in one line with Ca2+ and ATP [2,3]. It became clear that H2O2 serves fundamental regulatory functions in metabolism beyond the role as damage signal [4]. The metabolic and regulatory role of this oxygen metabolite has been increasingly recognized [5]. It serves as a key molecule in the Third Principle of the Redox Code, which is: “Redox sensing through activation/deactivation cycles of H2O2 production linked to the NAD and NADP systems to support spatiotemporal organisation of key processes” [6]·H2O2 occurs in normal metabolism in mammalian cells [7] and is a key metabolite in oxidative stress (see [8]). The general concept of eustress vs. distress was formulated in Refs. [15,16]
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