Mailing List Archive Mailing List Archive
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
--
Send mail for the `techdiver' mailing list to `techdiver@aquanaut.com'.
Send subscribe/unsubscribe requests to `techdiver-request@aquanaut.com'.
Navigate by Author:
[Previous]
[Next]
[Author Search Index]
Navigate by Subject:
[Previous]
[Next]
[Subject Search Index]
[Send Reply] [Send Message with New Topic]
[Search Selection] [Mailing List Home] [Home]