Re: Hey Pat: About nitric oxide

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Hey Mary, sorry for the delay. I have learned so much more
lately and have been having many discussions with doctors.

Martin Pall proposed that MCS is caused by NO poisoning. The
poisoning from NO is said to lead to neural sensitization, which
then produces MCS. The theory is fascinating.

Pall lists 10 facts that support his theory.

Quote:

1. Several organic solvents thought to be able to induce MCS,
formaldehyde, benzene, carbon tetrachloride and certain
organochlorine pesticides all induce increases in nitric oxide
levels.

2. A sequence of action of organophosphate and carbamate
insecticides is suggested, whereby they may induce MCS by
inactivating acetylcholinesterase and thus produce increased
stimulation of muscarinic receptors which are known to produce
increases in nitric oxide.

3. Evidence for induction of inflammatory cytokines by organic
solvents, which induce the inducible nitric oxide synthase
(iNOS). Elevated cytokines are an integral part of a proposed
feedback mechanism of the elevated nitric oxide/peroxynitrite
theory.

4. Neopterin, a marker of the induction of the iNOS, is reported
to be elevated in MCS.

5. Increased oxidative stress has been reported in MCS and also
antioxidant therapy may produce improvements in symptoms, as
expected if the levels of the oxidant peroxynitrite are elevated.

6. ?.. [See ANIMAL DATA]

7. The symptoms exacerbated on chemical exposure are very
similar to the chronic symptoms of CFS (1) and these may be
explained by several known properties of nitric oxide,
peroxynitrite and inflammatory cytokines, each of which have a
role in the proposed mechanism.

8. These conditions (CFS, MCS, FM and PTSD) are often treated
through intramuscular injections of vitamin B-12 and B-12 in the
form of hydroxocobalamin is a potent nitric oxide scavenger,
both in vitro and in vivo.

9. Peroxynitrite is known to induce increased permeabilization
of the blood brain barrier and such increased permeabilization
is reported in a rat model of MCS.

10. 5 types of evidence implicate excessive NMDA activity in
MCS, an activity known to increase nitric oxide and
peroxynitrite levels.

-- END QUOTE

The above is taken from "Multiple Chemical Sensitivity - The
End of Controversy" by Dr. Martin L. Pall, Professor of
Biochemistry and Basic Medical Sciences, Washington State
University, at
http://molecular.biosciences.wsu.edu/Faculty/pall/pall_mcs.htm

Pall can be contacted by phone at 509-335-1246.

Not mentioned in his essay, is the fact that the Gulf War
combatants who became ill and complain of chemical sensitivity
were administered pyridostigmine, which is metabolized by PON1.
However, the ill veterans were deficient of PON1 and thus their
bodies could not metabolize the pyridostigmine. Pyridostigmine
inhibits acetylcholinesterase, thus increases Acetylcholine,
which then increases NO levels.

Your question was an excellent one. I believe some are
predisposed to NO poisoning. Recently the AAAAI reported a high
incidence of the cholecystokinin B receptor allele 7---CCK-B
receptor--- in MCS sufferers. This genetic linkage is associated
with predisposition to "panic disorder." Thus, the researchers
concluded MCS is most likely a panic disorder. Setting aside the
problem of labeling such a psychogenic, CCK-B receptor modulates
NMDA activity, which just so happens to increase NO levels.
Thus, the study actually supports Martin Pall?s theory of MCS?s
etiology/ mechanisms (Pall, 2002). So what we appear to have is
a genetic predisposition to MCS.

ANIMAL DATA:

In Johnson?s documentary, Ashford and Bell discuss the animal
research on MCS. It turns out, that if you expose animals to the
very same chemicals reported to induce MCS in humans, then the
animals often develop chemical sensitivity.

Even large, powerful animals such as horses can develop chemical
sensitivity (reported by ACTA, 1999?see
http://whis.nzl.org/snftaas/pt20.html).

Martin Pall wrote, "In a series of studies of a mouse model of
MCS, involving partial kindling and kindling, both excessive
NMDA activity and excessive nitric oxide synthesis were
convincingly shown to be required to produce the characteristic
biological response." ("?End of Controversy") In other words,
animals cannot develop MCS without excessive levels of nitric oxide.

What are we to make of this data? Can we seriously say with a
straight face that chemically sensitive animals are simply
depressed, or are faking? Perhaps Ronald Gots could explain this
someday.

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