Effects of hyperbaric oxygen therapy on mitochondrial properties

Mitochondria are an important organelle responsible for providing energy to cells through the production of ATP. It also mediates cellular processes such as apoptosis and proliferation, and is involved in neuronal functions such as synaptic plasticity.

Mitochondria produce ATP through an electron transport chain in which oxygen plays an important role as the last electron acceptor in the chain. In this process, a proton gradient is created when protons are pumped from the mitochondrial matrix to the intermembrane space. The high concentration of protons in the intermembrane space creates an electrical potential and a chemical gradient of protons in the membrane, which is essential for maintaining the membrane potential and the ATP production process. When membrane integrity is compromised, apoptotic pathways are initiated within the cell.

I. Treatment of disease with hyperbaric oxygen

In neurons, there is a great need for well-functioning mitochondria because neuronal activity consumes a lot of energy and neurons have few energy reserves. Although several conditions may lead to mitochondrial dysfunction, such as mutations in mitochondrial DNA that amplify with age, the function of this organelle is heavily dependent on oxygen consumption. Decreased oxygen levels, such as hypoxic states, can impair energy production and lead to lactate accumulation in tissues as well as other metabolic changes. Therefore, some studies have considered the use of hyperbaric oxygen therapy treatment to treat neuronal disorders associated with mitochondrial dysfunction by increasing the amount of oxygen reaching the mitochondria.

II. hyperbaric oxygen therapy treatment helps to correct mitochondrial abnormalities

Hyperbaric oxygen therapy treatment helps correct mitochondrial abnormalities, such as those in mitochondrial metabolism, improves the integrity of damaged mitochondrial membranes, and inhibits secondary cell death by causing mitochondrial transfer from astrocytes to neurons. Several studies have measured the effects of hyperbaric oxygen therapy treatment based on changes in ATP levels after treatment. For example, Hu et al. studied a rat stroke model that was transformed by middle cerebral artery occlusion combined with hyperglycemia-induced ischemia and hemorrhage.

After hyperbaric oxygen treatment, ATP expression levels were measured by enzyme-linked immunosorbent assay, which showed a significant upregulation of ATP expression along with an increase in NAD+ expression, an important marker of energy metabolism. In addition, they observed an increase in the activity of nicotinamide phosphoribosyltransferase, a production-limiting protein for NAD+, and an upregulation of Sirt1 expression, an upstream protein of p53 and NF-κB, which are associated with apoptosis and inflammation, respectively. The simultaneous decrease in p53 and NF-κB expression reinforces the fact that the ATP/NAD+/Sirt1 pathway has been hyperbaric oxygen therapy treatment activated. Furthermore, administration of NAD+ exhibited effects similar to those of hyperbaric oxygen treatment, whereas administration of ATP synthase inhibitors, NAMPT inhibitors, or Sirt1 small interfering RNA prevented the positive effects of hyperbaric oxygen therapy treatment. activation of this specific pathway by hyperbaric oxygen therapy treatment reduced cell necrosis and improved neurological function.