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The aim of the research part of my PhD is to look further into some of the biochemical reactions linked to decompression sickness. Tetrahydrobiopterin (BH4) is an essential cofactor of the enzyme Nitric Oxide Synthase (NOS). NOS produces Nitric oxide (NO), a signal molecule responsible for vasodilation, and its bioavailability is important for endothelial function. What happens to the NOS enzyme, and NO production, when its cofactor (BH4) is oxidized during a dive? How can this be related to decompression sickness? Are there potent antioxidants that can maintain the bioavailability of BH4? These are questions I am trying to find the answer to.
My PhD is part of a project titled; "Tetrahydrobiopterin as a key factor in the pathophysiology of diving". Keywords: BH4, hyperoxia and diving.
Oral presentation at the European Underwater and Baromedical Society conference in Geneva, September 2016.
Oral presentation (in Norwegian) at the Autumn meeting for the Norwegian Baromedical Society, September 2016.
- 2019. Hyperoxia and lack of ascorbic acid deplete tetrahydrobiopterin without affecting NO generation in endothelial cells. Undersea & Hyperbaric Medicine. 46: 509-519.
- 2019. Decrease of tetrahydrobiopterin and NO generation in endothelial cells exposed to simulated diving. Undersea & Hyperbaric Medicine. 46: 159-169.
- 2019. Tetrahydrobiopterin and nitric oxide synthesis after exposure to hyperoxia and simulated diving. An experimental study in human endothelial cells and healthy humans. Universitetet i Bergen.