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Predictions of Multiple Chemical Sensitivity Mechanism Confirmed by Roman Study

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Predictions of Multiple Chemical Sensitivity Mechanism

Confirmed by Roman Study

 

FOR IMMEDIATE RELEASE

 

Portland, OR – July 5, 2010 - The physiological mechanism for

Multiple Chemical Sensitivity proposed by biochemist L. Pall has been

confirmed with the recent findings of an independent research group in Rome.

 

Multiple chemical sensitivity (MCS), also known as chemical

sensitivity and toxicant-induced loss of tolerance (TILT), is a disease

initiated by toxic chemical exposure, leading to toxic brain injury that

produces high level sensitivity to the same set of chemicals that are implicated

in initiation of the disease. 

Sensitivity responses in other areas of the body are also often

seen.

 

“Epidemiological studies show that MCS is a stunningly common

disease, even more common than diabetes,†said Pall, professor emeritus of

biochemistry and basic medical sciences at Washington State University. “My

review of the literature and other research I’ve conducted over the past

eleven

years shows the probable central mechanism of MCS is a biochemical vicious

mechanism, known as the NO/ONOO- cycle.â€Â Â Â 

 

Pall’s work is widely published in books and articles, the most

recent of which is a chapter in the authoritative international reference

manual  for professional

toxicologists, General and Applied

Toxicology, 3rd Edition, 2009. 

 

The NO/ONOO- cycle

 

The NO/ONOO- cycle, pronounced no-oh-no, is named for the chemical

structures of nitric oxide (NO) and peroxynitrite (ONOO-). This biochemical

vicious cycle mechanism predicts that each of the elements linked together in

the cycle are elevated in patients suffering from MCS and related diseases. Most

of the elements of the cycle have been shown to be elevated in such related

diseases as chronic fatigue syndrome and fibromyalgia and also in animal models

of MCS.  However, several cycle

elements have never been measured in MCS patients. 

 

The recent study conducted by the research group in Rome is

significant in regard to the NO/ONOO- cycle theory because it shows that three

elements of the cycle are elevated in MCS patients (De Luca et al, Toxicology

and Applied Pharmacology,

2010, April 27 Epub ahead of print). Those elements are the inflammatory

cytokines, nitric oxide, and oxidative stress. Each of these measurements

provides important confirmation of the disease mechanism proposed by Pall.

 

The inflammatory cytokines and nitric oxide elevation have never

before been measured in MCS patients, although they have been shown to be

elevated in animal models of MCS. Oxidative stress has been reported in two

earlier studies of MCS patients, but the data provided in the De Luca et al

study are much more extensive than are the earlier data. Consequently, these new

data all provide important confirmation of the NO/ONOO- cycle as the central

disease mechanism in MCS.

 

The NO/ONOO- cycle also is useful in understanding the role of

toxic chemicals in MCS and the role of treatment. Each of the seven classes of

chemicals implicated in MCS are thought to act indirectly to increase the

activity of the NMDA receptors, which are glutamate receptors for controlling

synaptic plasticity and memory

function. This activity, in turn, leads to rapid increases in intracellular

calcium (Ca2+), nitric oxide and peroxynitrite (ONOO-), acting to

greatly stimulate the NO/ONOO- cycle.

 

“Many of the agents used by environmental medicine physicians to

treat MCS patients can be viewed as lowering different parts of the cycle, and

thus are validated in part by this mechanism,†Pall said.  “Consequently,

the NO/ONOO- cycle

mechanism can be viewed as validating therapeutic approaches used in

environmental medicine in the U.S., in Germany and some other areas of Europe

and in some other countries.â€

 

Contact:

L. Pall, PhD 

Professor Emeritus of Biochemistry and Basic Medical Sciences

Washington State University

503-232-3883

martin_pall@ wsu.edu

thetenthparadigm. org

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