The Role of Mitochondria in Ozone Therapy

Abstract

Inhaled ozone can react with the biomolecules present in the epithelial lining fluid, causing the depletion of antioxidants. It can react with the surfactant polyunsaturated fatty acids (PUFA) present at the air-ELF interface to form several reactive oxygen species (ROS). High ozone exposure resulted in sustained ventricular tachycardia in male and female rats. Ozone can induce oxidative stress, alter some inflammatory factors in tissue, and induce mitochondria-dependent apoptosis. It is not surprising that the mitochondria could be putatively affected by ozone as this organelle is highly sensitive to oxidative stress. Exposure of blood to a few micrograms of ozone was shown to cause a decrease in mitochondrial function and energy metabolism, as it caused a decline in ATP levels and an increase in the NADH/NAD+ ratio. It was also found that cytochrome-c-oxidase was almost wholly inhibited under these conditions. However, in a specific range of concentrations, ozone can induce a beneficial modulation in the anti-inflammatory and antioxidant systems. Some of the biological responses induced by ozone may be potentially suitable to become an active part of the various mechanisms of metabolic regulation, with positive effects on several pathologies. The therapeutic efficacy of ozone therapy may result from controlled and moderate oxidative stress produced by ozone’s reactions with various biological components. Although there is not enough data, there are indications that ozone may induce good responses in mitochondria.