Clinical evidence of ozone interaction with pain mediators.

OBJECTIVE: To address the clinical evidence that may support the fact that subcutaneous administration of ozone (O3) has anti-hyperalgesic effects probably acting by modifying specific pain targets. METHODS: Fifty-two patients attending the Medinat Clinic, Camerano, Ancona, Italy between October 2004 to October 2009 were eligible to participate in the study. Panoramic photos of painful and not painful areas submitted to oxygen (O2)/O3 ozone treatment injection were analyzed to detect the intensity of erythema. RESULTS: The erythematic areas after O3 subcutaneous puncture showed significant (p<0.05) increment (83 ± 5%) in the painful area versus 7 ± 6% in the contralateral area. CONCLUSION: The surrounding erythema observed during O3 intervention should explain at least in part, its interaction with some pain mediators. This may involve algesic mediators or receptors. The analgesic mechanism induced by O2/O3 may involve 2 independent steps: a short-term mechanism that may correspond with the direct oxidation on biomolecules, and a long-term mechanism that may involve the activation of antioxidant pathways. Further studies are needed to support the biochemical analgesic mechanism of O3 therapy.

Ozone therapy: clinical and basic evidence of its therapeutic potential.

Ozone has recently been subjected to criticism and emphasis in relation to clinical efficacy and toxicity, respectively. Without a doubt, ozone, in common with oxygen itself, is one of the most potent oxidants. Ozone is considered one of the major pollutants in urban areas. Nevertheless, increasingly widespread use lately has highlighted the potential benefits as a therapeutic agent when used according to well-defined and safe protocols. Basic studies conducted following rigorous scientific and ethical criteria have been proposed for scientific discussion. This paper concerns original data on an in vivo model of Parkinson's disease and published data on the effect of low ozone doses with any risk of toxicity excluded with the concentrations commonly used in medical applications.

Role of protein synthesis in the protection conferred by ozone-oxidative-preconditioning in hepatic ischaemia/reperfusion.

The liver is damaged by sustained ischaemia during liver transplantation, and the reperfusion after ischaemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischaemia/reperfusion (I/R) injury through different mechanisms. The aim of this study was to investigate the influence of the inhibition of protein synthesis on the protective actions conferred by OzoneOP in hepatic I/R. Rats were treated with cycloheximide (CHX) in order to promote protein synthesis inhibition after OzoneOP treatment. Plasma transaminases, malondialdehyde and 4-hydroxyalkenals and morphological characteristics were measured as an index of hepatocellular damage; Cu/Zn-superoxide dismutase (SOD), Mn-SOD, catalase, total hydroperoxides and glutathione levels as markers of endogenous antioxidant system. OzoneOP increased Mn-SOD isoform and ameliorated mitochondrial damage. CHX abrogated the protection conferred by OzonoOP and decreased Mn-SOD activity. Cellular redox balance disappeared when CHX was introduced. Protein synthesis is involved in the protective mechanisms mediated by OzoneOP. Ozone treatment preserved mitochondrial functions and cellular redox balance.