Quote from Ourania on February 1, 2026, 12:25 pm

EBOO (Extra-coeporeal Blood oxygenation and ozonation). Has anyone tried it?

Supposed to destroy retinoic acid in blood serum :

in: Extracorporeal blood oxygenation and ozonation: clinical and biological implications of ozone therapy :   N. Di Paolo, E. Gaggiotti, F. Galli:

Unlike the respiratory system, the components of human blood are in a dynamic state and they can neutralise the oxidising power of ozone by means of specific defence systems. Like other gases (i.e. O2, CO2), ozone must be dissolved in water in order to interact with organic substrates. In blood, it dissolves in plasma and instantly decomposes in a cascade of reactive oxygen species (ROS), including hydrogen peroxide (H2O2), superoxide anion (O₂^•−), hydroxyl radical (HO•) and hypochlorous acid (HClO). ROS are normally produced during several processes of physiological relevance such as cell respiration by mitochondria, the respiratory burst that accompanies phagocytosis and xenobiotic detoxification, being also important cell messengers and gene transcription regulators.16,17 Some of these species are highly reactive compounds with a short half-life, therefore, representing potentially toxic compounds that may affect different biochemical targets leading to the formation of reactive by-products and molecular lesions. Repair or elimination by metabolic processing and/or excretion are key responses of living organisms to the ROS- (and thus ozone) dependent damage to biomolecules.

 

 

from chatgpt:

All four oxidants modify retinoic acid (RA) in human serum but by different mechanisms: H₂O₂ is a relatively weak direct oxidant (needs catalysts/peroxidases), superoxide mainly initiates secondary oxidation, the hydroxyl radical (HO•) causes very fast, non‑selective fragmentation and hydroxylation, and hypochlorous acid (HOCl) is a powerful electrophile that chlorinates/cleaves the conjugated polyene of RA. In serum these reactions are strongly modulated by albumin, glutathione, and enzymatic peroxidases, so net RA loss and product profiles depend on antioxidant capacity and metal catalysts. 

 

Hydroxyl radical (HO•)

Mechanism: Extremely reactive and non‑selective; attacks double bonds, causing hydroxylation, cleavage, and fragmentation of RA almost at diffusion‑limited rates. 

Outcome: Rapid loss of RA and formation of multiple small oxidation products; even low HO• fluxes produce significant RA degradation.