The Role of Mitochondria in Ozone Therapy

Background: why mitochondria matter in ozone therapy

Mitochondria are the cell's main energy producers and act as a central hub for redox signalling - the balance between oxidising and antioxidant molecules that keeps cellular processes in check. Because medical ozone works by delivering a brief, controlled oxidative challenge, researchers have long suspected that mitochondria are one of its key targets. This mini-review sets out to gather what the preclinical evidence says about how ozone influences mitochondrial function and redox balance, and where the gaps still lie.

What this review covers

The article is a narrative mini-review rather than a systematic one: the authors summarise and interpret published work without pooling data or formally scoring study quality. The evidence they draw on is largely preclinical, coming from laboratory (in vitro) experiments and animal models rather than clinical trials in people. Across these studies, ozone is administered at different concentrations and by different routes, and its effects are assessed on markers of mitochondrial activity, oxidative stress and the cell's own antioxidant defences.

Findings: a non-linear, dose-dependent effect

A consistent theme is that ozone's effects do not follow a straight line with dose. Very low concentrations appear to do little, while low-to-medium concentrations are associated with beneficial effects - including activation of the body's endogenous antioxidant systems and support for mitochondrial function and redox balance. High concentrations, by contrast, can be harmful, producing effects opposite to those seen at more moderate doses. This pattern, in which a mild stressor prompts a protective adaptive response, is characteristic of hormesis. The authors note that the outcome in any given study also depends on the duration of treatment, the route of exposure, the target organ and the particular animal model used.

What the authors concluded

The authors conclude that there is now considerable evidence that ozone can modulate mitochondrial function and redox balance, even though the precise molecular mechanisms are not yet fully understood. They stress that understanding the relationship between ozone and the body's own antioxidants is essential for defining the appropriate concentration to administer, given that the effect is non-linear. They call for further studies using a range of animal models, concentrations and routes of administration to clarify the mechanisms underlying the effects observed on mitochondria.

Limitations of this review

This is a narrative mini-review, so it does not use the systematic search, quality appraisal or data pooling of a systematic review, and selection of the cited studies is at the authors' discretion. The underlying evidence is mechanistic and preclinical - drawn from cell and animal experiments - so it describes biological pathways rather than clinical outcomes in patients, and the beneficial doses identified in the laboratory cannot be read directly across to human treatment. The authors themselves highlight that the mechanisms remain incompletely understood and that results vary with concentration, route, treatment duration, target organ and animal model. The findings should therefore be read as a summary of proposed mechanisms and a case for further research, not as evidence of clinical benefit.