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    Re: Hey Pat: About nitric oxide

    Posted by Hey on 4/28/03

    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.


    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

    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

    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

    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.


    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

    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

    Posts on this thread, including this one

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