Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress.
Level 5 - mechanism / opinion, no new human data
Narrative review of biochemical mechanisms without primary human clinical data
PubMed 28110218 · doi:10.1016/j.redox.2016.12.035
What was done
This narrative review summarizes metabolic sources, sinks, assay methods, and concentration-dependent signaling pathways of hydrogen peroxide (H2O2) in biological settings.
What was found
The abstract reports defined concentration windows for H2O2 activity: physiological redox signaling (oxidative eustress) occurs at 1–10 nM; higher concentrations trigger adaptive stress responses via pathways like Nrf2/Keap1 or NF-κB; and supraphysiological concentrations (>100 nM) cause biomolecular damage (oxidative distress).
Why it matters
It distinguishes beneficial physiological redox signaling from pathological oxidative damage based on specific nanomolar concentration thresholds.
Limits
As a narrative overview, it provides no systematic search methodology, meta-analytic pooling, or new empirical human data. Context-specific in vivo variations and assay limitations are not detailed in the abstract.
Cited by
- supports Reactive oxygen species (free radicals) function as essential signaling molecules within cells and participate in adaptive cellular responses to stress.