2024/10/22 by Ondřej Groborz, Petr Maršálek, Luděk Šefc · 1 voice
Biochemistry, Genetics and Molecular Biology · Pharmacology, Toxicology and Pharmaceutics · #Caveolin-1 and cellular processes #Mitochondrial Function and Pathology #Plant-based Medicinal Research
paper · doi:10.1016/j.lfs.2024.123169
openalex publication_date 2024/10/22 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/25
Hyperbaric oxygen therapy (HBOT) elevates the partial pressure of life-sustaining oxygen (pO 2 ), thereby saving lives. However, HBOT can also cause toxic effects like lung and retinal damage (peripheral oxygen toxicity) and violent myoclonic seizures (central nervous system (CNS) toxicity). The mechanisms behind these effects are not fully understood, hindering the development of effective therapies and preventive strategies. Herein, we critically reviewed the literature to understand CNS oxygen toxicity associated with HBOT to elucidate their mechanism, treatment, and prevention. We provide evidence that (1) increased pO 2 increases reactive oxygen species (ROS) concentration in tissues, which irreversibly alters cell receptors, causing peripheral oxygen toxicity and contributing to CNS oxygen toxicity. Furthermore, (2) increased ROS concentration in the brain lowers the activity of glutamic decarboxylase (GD), which lowers concentrations of inhibitory neurotransmitter γ -aminobutyric acid (GABA), thereby contributing to the onset of HBOT-derived seizures. We provide long-overlooked evidence that (3) elevated ambient pressure directly inhibits GABA A , glycine and other receptors, leading to the rapid onset of seizures. Additionally, (4) acidosis facilitates the onset of seizures by an unknown mechanism. Only a combination of these mechanisms explains most phenomena seen in peripheral and CNS oxygen toxicity. Based on these proposed intertwined mechanisms, we suggest administering antioxidants (lowering ROS concentrations), pyridoxine (restoring GD activity), low doses of sedatives/anesthetics (reversing inhibitory effects of pressure on GABA A and glycine receptors), and treatment of acidemia before routine HBOT to prevent peripheral and CNS oxygen toxicity. Theoretically, similar preventive strategies can be applied before deep-sea diving to prevent life-threatening convulsions.