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Chuck,
As to the possible evolution of a process that would protect against free
radicals etc., I would want to discuss the process of random oxidative
metabolism, as a byproduct to aerobic level exertions, particularly of
frequent or long duration ( the type which would build more destructive
levels of free radicals, and would certainly have effected the survival
ability on prehistoric man, as well as his predecessors right down to the
"fury little mammals":-).
Buffers, scavengers and various enzyme systems related to this all have
multiple functions. Protection against high PO2 levels is most likely just
one more instance of a biological condition of no usefulness in an
evolutionary sense, until some catastrophic event causes it to have
competitive survival advantage in a population. Never the less, it would
appear to have a high likelihood of function in this direction, even though
next to zero chance exists for it to ever become an evolutionary adaptation
in humans.
Hyperbaric exposures with advanced nutritional products (to maximize
antioxidizing potential) need to be among the issues we spend more time
investigating in the coming year.
Regards,
Dan Volker
-----Original Message-----
From: CHKBOONE@ao*.co* [mailto:CHKBOONE@ao*.co*]
Sent: Friday, November 27, 1998 10:01 AM
To: techdiver@aquanaut.com
Subject: Re: 80% arrrgh!! was Re: On the left
In a message dated 11/26/98 9:34:40 PM Eastern Standard Time,
ebeaule@gl*.ne* writes:
> Long exposure to high PO2 will cause a depletion
> of the molecules involved in the protection mechanism (oxygen scavenger
> and other name of the sort are used to describe these molecules). Once
> you have depleted all your defenses, oxygen will be free to cause some
> damage to the tissues... but this is not likely to occur with brief
> exposures.
>
> But again, if you use good deco techniques, you can prevent most of the
> PO2 shifts.
>
> Etienne
>
---------------------------------------------------
Not to take either side here (yet) but . . . on the other side of the coin
we have divers who have no problems with extremely high O2 exposures one day
and take a hit on moderate exposure another day. I seem to remember
reports
of rare occasions of people toxing in hospitals on 1 ata - CNS.
I find your reference to "Oxygen Scavengers" interesting. I cannot
picture a mammal such as ourselves evolving a defense mechanism against
something so unlikely to encounter in our natural environment as high O2.
Chances are that the binding of O2 is not the drive behind the evolution of
these "scavenger" molecules, rather that they normally facilitate an
entirely
different function and this is a coincidental event - probably detrimental
to
the blood and systemic chemistry.
Also there is a big difference between binding to a free radical (singlet
O2) and capturing a diatomic gas molecule. Which are you saying these
scavengers do?
If these "scavengers" are in place and capture diatomic O2 how does O2 get
past them to enter the cells after dissociating from Hb and how long would
the
processes of normal respiration take to deplete these defense molecules?
If
they only bind to singlet O2 what process breaks down the O2 molecule to
make
the radical available.
How do you figure that brief exposures will be benign considering the
rate
at which chemical reactions occur in the blood if these toxicity problems
stem
from such events as the depletion or overwhelming of defensive chemistry ?
Lest this start another thread on O2 radicals note that there is so much
plasma bound O2 available to the system on air at one atmosphere that the
addition of a few zillion more molecules, as when diving, would probably
kill
us in short order by total destruction of the blood chemistry if it
contributed to the production of more radicals.
All this extra O2 just goes along for the ride in the blood as a diatomic
molecule without being broken into dangerous radicals. Though the
mechanisms
of toxicity problems is not well understood I think it is safe to assume
that
both CNS & OTU toxicity result from localized interactions with the diatomic
form, not from widely dispersed radicals in the blood or tissues.
Chuck Boone
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