Hyperbaric oxygen treatment (HBOT)-the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA-increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion-the organelle that consumes most of the oxygen that we breathe-at the epicenter of HBOT's effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.
Keywords: HIF1a; Nrf2; SIRT1; hyperbaric oxygen treatment (HBOT); hyperoxic–hypoxic paradox; mitochondrial function; neuroinflammation; oxidative stress; reactive oxygen species (ROS); superoxide dismutase (SOD).