Revisiting the often overstated topic of oxygen toxicity and oxidative stress at the cellular level, today’s paper and sharing of the work of others addresses, as a few other recent ones have, that HBOT provides it’s own protective mechanisms against oxidative stress caused by reactive oxygen and nitrogen species (RONS).
It is established that hyperbaric oxygen therapy increases and triggers a greater occurrence of RONS in the bloodstream and tissues and for a long time this was considered a hazardous condition capable of damaging intra cellular structures including DNA. In fact it was the primary argument cited when the case was made against HBOT and other oxygen therapies. In cases where RONS are upregulated by other causes and without HBOT, this can indeed be the case. Oxygen free radicals, being reactive oxygen molecules, derive from this and are indeed dangerous to tissues and cells. This definition applies to oxygen free radicals:
Oxidative stress occurs when an oxygen molecule splits into single atoms with unpaired electrons, which are called free radicals. Electrons like to be in pairs, so these atoms, called free radicals, scavenge the body to seek out other electrons so they can become a pair. This causes damage to cells, proteins and DNA .
Notwithstanding that, an increasing evidence base is beginning to overturn this thinking as it applies to HBOT since studies and experiments in vitro and in vivo show that following the first hyperbaric oxygen treatment, antioxidant response is up-regulated and not only is any damage immediately repaired but HBOT provides an ongoing protective mechanism throughout the balance of and following treatment.
This is because RONS and specifically reactive oxygen species (ROS), have been found to be significant signaling molecules, which signal the upregulation of the antioxidant response.
In other articles we discuss transcription factors and signalling proteins which signal various biological responses in the body. In a similar way, ROS act as powerful signallers, triggering antioxidant responses which more than adequately protect against any free radical action previously thought to be a limiting factor to HBOT.
Additionally, today’s short peer reviewed paper addresses specifically diabetic patients who are more susceptible to ROS damage which can affect the metabolic function of cells. ROS is part of the mechanism which is thought to affect the insulin response of cells in type 2 diabetes. Diabetes, specifically type 2 diabetes and wound healing, is of particular interest to us following various articles and proposals authored thus far. As a type 2 diabetic myself, it is in my interest to further any therapy than can benefit sufferers including myself. This is more than lip service. This paper goes a long way to reassuring diabetic sufferers of the benefit HBOT can have to wound healing while creating no additional problems.
The paper concludes:
“In conclusion, this study supports the view that HBO triggers and upregulates the defense mechanism against oxidative stress. Increased oxygenation of tissues due to HBOT may also activate other endogenous factors that prevent hazardous effects of the disease itself. [diabetes] In Addition, it is now evident that drugs such as statins and ACE inhibitors [cholesterol and blood pressure medication] have a strong intracellular antioxidant activity, and may therefore exert beneficial effects on diabetic vascular complications (Tsiaraet al. 2003, DaRos et al.2004). The contribution of these drugs to the healing effect of HBO needs to be elucidated by further studies.“
The paper can be found on the references page but is linked here also for convenience: It is entitled:
A good read and not over the top in scientific terms.