Hello, Once again I apologize for being much further behind schedule than I expected with continuing this discussion. This one is a little verbose and may not be completely written in "layman's" terms. Enzymes have been a hotly debated, and misunderstood by most, topic in regards to oxygen toxicity. In the last post I attempted to shed some light on the basics of pulmonary toxicity in hopes that we would all be starting this next round of discussions on the same level. Hyberbaric oxygen (HBO) should be viewed as a necessary evil for what we do. Without it (by this I mean altered concentrations) we would be in the water for days, too much of it and we may die, either a rapid and mostly painless death, or by a slow and lingering "suffocation" (and/or drowning in our own fluid) from hypoxia. A careful balance must be stuck between the good and the bad; all of this is common sense (the application, not the explanation) and it is our hope that by disclosing/discussing information that many people will learn. Oxygen toxicity, as well as increased exposure, increases the production of highly reactive, partially reduced metabolites of oxygen that include free radicals and hydrogen peroxide; these arise within the mitochondria as oxygen is reduced to water. Oxygen free radicals play a primary role in the pathophysiology of oxygen toxicity. Free radicals are implemented in microbiological theories on aging and are known to reek havoc on DNA and cellular structures by ricocheting around inside the cell, leading to problems such as cancer and arthritis. Superoxide anion is the most commonly produced radical which will breakdown into hydrogen peroxide. Hydrogen peroxide is capable of diffusing through cell membranes, will react with transition metals and produce a highly reactive hydroxyl radical. Hydroxyl radicals in turn set of chain reactions of lipid peroxidation that lead to cell rupture. Damage is caused and/or exacerbated by the production of free radicals and other oxygen metabolites are formed at rates that exceed the cells natural antioxidants defense mechanisms to detoxify them. There exist some enzymatic intracellular defense mechanisms which are designed to protect cells from the toxic effects of free radicals. Protection may also rely on the synthesis of antioxidant enzymes, nitric oxide production, modulation of alveolar macrophages activity and the recruitment of neutrophils. The antioxidant enzymes, which include superoxide dismutase, glutathione peroxidase, and catalase, and cellular antioxidants can scavenge the free radicals and repair the damaged lipids; however, this is only against normal levels of radicals. As divers using oxygen we produce much more and thereby overwhelm the system to a greater degree. Damage is also caused by pulmonary lesions, this is believed to be related to free radical production. Some of the protective enzymes mentioned above, as well as non enzymatic systems and vitamins C and E, and glutathione, are capable of preventing lesions that are cause be radicals. Lesions are often the result of long-term and repeated exposures. Once all of this damage is underway this is massive inflammatory response of the airways and interstitiums of the lungs. This leads to some of the stiffness that has been discussed in prior post by others; it also leads to an increase in the diffusion distance between the alveoli and the capillaries, which in turn leads to hypoxia due to the high levels of oxygen. While breathing HBO mixes our system will become saturated w/ oxygen and past this point we derive no benefit from breathing high pO2 mixes: all we do from saturation on is create more radicals and this in turn creates more damage. BACK GAS BREAKS are the mechanism that we use to prevent from going over the saturation curve, remember there is no benefit beyond it, and decreasing the risk. While breathing the BG our cellular oxygen levels drop and our returning to the higher pO2 mix is merited. There currently exist no pharmacological "fix" for pulmonary toxicity, although there is some promising enzyme, as well as other, treatments in the works. For now the only way to handle this problem is to use the right gas at the right depth, take proper pre-dive precautions (some recommend vitamins, antioxidants, free radical "fighters" etc), and judicious use of BG breaks. I hope that this may have answered some of the questions regrading toxicity, if it created more questions then that is fine too. The next post I will put out will deal with back gas breaks. The why of BG breaks has been covered, so I plan on covering the how, when, etc. Sincerely, Scott Hunsucker
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