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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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