How ozone works
By Dr. med. Gerd Wasser
The chemical reaction between ozone and organic double bonds has been known about since 1904. Its structure was postulated in the 1920s and in the 1950s it was finally confirmed through chemical analysis. First, primary ozonides are formed which are highly explosive in anhydrous environments. These then spontaneously decay into secondary, stable ozonides (Lit. 1, 2).
For ozone treatment, this means a reaction that takes place in microseconds with cell membranes which contain unsaturated fatty acids as part of their membrane lipids. In the hydrophilic environment of the lipid double layer, this therefore creates a hydrophilic island which, due to the repulsive forces in the aqueous environment, is forced out of the membrane and primarily into the cell’s cytoplasm, but also into the interstitium. This process is similar to that of lysophosphatide formation, which causes membrane lysis or irreversible changes to erythrocytes such as echinocytogenesis. At the low doses required for ozone to have an effect, these processes are not relevant (Lit. 3,10).
In chemical terms, ozonides belong to the peroxides, which have a special protective system against oxidative damage to individual cell compartments known as the glutathione peroxidase reductase system. This selenium-containing enzyme system (of which there is also a selenium-free version) regenerates the used glutathione which acted as a the H ion donor and clustered together to form GSSG. As a result of the lysis of GSSG by the glutathione reductase, hydrogen is once again required. The provider in this case is NADPH, which is produced as NADP* from this reaction. DANPPH is then regenerated via the pentose shunt and glycolysis.
Glycolysis, however, produces ATP, which starts the actual mechanism of effectiveness for ozone treatment. The drainage of full ATP stores in erythrocytes as a substitution for starved tissue is described (Lit. 4). In this case, the erythrocyte’s enzyme pattern is neither modified nor damaged thanks to an adequate dose of ozone (Lit. 3).
Through the formation of ATP, ozone therefore has a strain-relieving effect on the respiratory chain, does not require the use of oxygen, but instead reduces oxygen requirements by between 20 and 25% (Lit. 4, 5, 6, 7). In this case, the usual treatment methods should not be used to address a tumour or virus-infected cell within the body, since the ozonides develop with the first membrane contact and then trigger the intracellular chemical reactions.
At local level, the situation is different. Bacteria are killed due to the oxidisation of the respiratory chain (which is positioned on the external-facing side of the cell membrane). It contains enzymes such as fumarate reductase and succinate dehydrogenase for the quinone formation in oxidation and reduction. These respiratory enzymes cross the cytoplasmic bacterial membrane (Lit. 11). 2Fe-2S ferodoxin and 7Fe-8S ferodoxin also act as electron acceptors, e.g. for NADPH.Cytochrome C, part of the III complex in the respiratory chain, is also positioned on the side facing the cytoplasma. It contains haem iron, the oxidisation of which interrupts the flow of protons and therefore the ATP synthesis taking place in complex V. This structure, which is essential for survival, is also extremely sensitive. Its oxidation leads to the immediate collapse of the metabolic process, since only inadequate quantities of ATP can be produced through glycolysis.Bacteria are therefore unable, unlike tumour cells, to compensate for the lack of ATP through the increased metabolism of glucose via glycolysis in a glucose-rich medium. This means that the oxidative damage to the respiratory chain is the trigger of cell death. The oxidative change to membrane lipids, enzymes and other macromolecules plays only a secondary role. This also explains why spores are relatively resistant to the effects of ozone. Spores do not immediately die due to severely – to the point that it becomes unquantifiable – reduced metabolism. It remains to be verified, however, just how much germination is inhibited or stopped following oxidation.
Mitochondria in the tissues, as supporters of the respiratory chain, are not damaged, however, since their reactions also take place in the outer cell membrane. Accelerated wound healing with simultaneous disinfection of the wound area therefore only appears to be a paradoxical process.
When carcinomas on the surface of the body or in the operation site are flushed with ozone, the ozone can kill the tumour cells, but only if they develop a GST (glutathione transferase) deficit. Multi-drug-resistant cells exhibit high levels of enzyme activity and therefore strong detoxification capacities vis-à-vis ROS (Reactive Oxygen Species) (Lit. 8).
These cells therefore benefit from the effect of ozone by reacting just like other cells with ATP production.
Routine irrigation of an operation site following tumour resection with ozone water is therefore not recommended. Hydrogen peroxide rinsing following tumour resection destroys the tumour cells, particularly in the presence of iron-containing enzymes, through the formation of hydroxyl radicals. However the surface of healthy tissue is also attacked. This process provides considerable protection against vaccine metastases (Lit. 9). Irrigation with ozone water is only justifiable after this treatment and will stimulate the regeneration of healthy tissue.