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?relationship btn pesticides, PON gene cluster variant, parkinson's and statins??????
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eml
medicine forum Guru Wannabe


Joined: 12 Jun 2005
Posts: 135

PostPosted: Thu Jul 06, 2006 11:17 pm    Post subject: ?relationship btn pesticides, PON gene cluster variant, parkinson's and statins?????? Reply with quote

---Low-dose pesticide exposure boosts Parkinson's risk by 70 percent


Originally published June 26 2006(NewsTarget) According to a study
published
in the July issue of Annals of Neurology, people who have been exposed
to
pesticides run a 70 percent higher risk of developing Parkinson's
disease
than people who aren't exposed to pesticides.
The study -- comprised of roughly 143,000 men and women -- ran from
1982 to
2001, tracking participants' responses to extensive lifestyle
questionnaires. At the beginning of the survey, none of the
participants
showed symptoms of Parkinson's. By the end of the survey, 413
participants
had developed the disease -- an occurrence strongly linked with being
occupationally or otherwise exposed to pesticides.


The study's lead author, Alberto Ascherio of the Harvard School for
Public
Health, said, "Low-dose pesticide exposure was associated with a
significant
increase in risk for Parkinson's disease. I think this is one reason to
be
careful about using pesticides in general."


Environmental factors have long been suspected as a cause of
Parkinson's,
and Ascherio's study is the first large-scale population study to prove
the
link, though the study's design did not allow for determining how the
duration, frequency or intensity of pesticide exposure influenced
development of the disease. However, the study was able to prove that
only
pesticide exposure -- not exposure to coal dust, asbestos, exhaust,
radioactive material or formaldehyde -- correlated with developing
Parkinson's. Ascherio says the next step is figuring out specifically
what
chemicals in those pesticides cause the disease.

REPORT #2:

Northwestern University
Variations in detoxifying genes linked to Lou Gehrig's disease
Genetic variations in three enzymes that detoxify insecticides and
nerve gas agents as well as metabolize cholesterol-lowering statin
drugs may be a risk factor for developing sporadic amyotrophic lateral
sclerosis (ALS, or Lou Gehrig's disease), and possibly responsible for
a reported twofold increased risk of ALS in Gulf War veterans.

These findings, from a study led Teepu Siddique, M.D., and colleagues
at Northwestern University, open the door to investigating
gene-environment interactions as a cause of ALS and other illnesses and

to the development of molecular targets for specific treatments. The
study was published in the August 22 online issue (available now) of
the journal Neurology.


Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor,
Davee Department of Neurology and Clinical Neurosciences, professor of
cell and molecular biology and director of the Neuromuscular Disorders
Program at Northwestern University Feinberg School of Medicine.


ALS is a complex neurodegenerative disorder of the motor neurons that
results in muscle weakness, difficulty speaking, swallowing and
breathing and eventual total paralysis and death generally within five
years.


In 1993 Siddique and collaborators determined that mutations in a gene
known as SOD1 account for 20 percent of familial, or inherited, ALS (2
percent of all cases of ALS). However, the cause of sporadic ALS is
still unknown.


In earlier research Siddique and other researchers hypothesized that
sporadic ALS is modulated by variations in multiple genes interacting
with each other and environmental exposures.


The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are
located on chromosome 7q21.3, code for the production of detoxifying
enzymes involved in the metabolism of a variety of drugs,
organophosphate insecticides, such as parathion, diazinon and
chlorpyrifos, and nerve gas agents such as sarin.


Previous research described a possible twofold increased risk for
developing ALS in veterans of the Gulf War, indicating a war-related
environmental exposure to organophosphates and sarin in genetically
susceptible individuals as a possible cause. PON gene cluster variants
have previously been associated with other neurodegenerative and
vascular disorders, including Alzheimer's disease, Parkinson's disease,

coronary artery disease and stroke.


Although the Northwestern DNA study samples were not analyzed for
inclusion of Gulf War veterans, Siddique and co-researchers found
significant evidence that gene variations (polymorphisms) on the
chromosome region encompassing PON2-PON3 were strongly associated with
sporadic ALS.


"Thus, single nucleotide polymorphism genotyping in the intergenic
regions of the PON gene cluster, and replication, gene expression,
gene-gene interaction and PON serum/enzymatic studies may help
elucidate the complexity of PON cluster association with ALS," Siddique

said.


Siddique hopes to study DNA samples from Gulf War veterans with
increased incidence of sporadic ALS and has applied for their DNA from
the Veterans Administration collection.


http://www.eurekalert.org/pub_releas...-vid070506.php
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William Wagner
medicine forum Guru


Joined: 29 Apr 2005
Posts: 809

PostPosted: Fri Jul 07, 2006 10:31 am    Post subject: Re: ?relationship btn pesticides, PON gene cluster variant, parkinson's and statins?????? Reply with quote

In article <1152227865.153896.121060@p79g2000cwp.googlegroups.com>,
"eml" <mmlevy46@hotmail.com> wrote:

Quote:
---Low-dose pesticide exposure boosts Parkinson's risk by 70 percent


Originally published June 26 2006(NewsTarget) According to a study
published
in the July issue of Annals of Neurology, people who have been exposed
to
pesticides run a 70 percent higher risk of developing Parkinson's
disease
than people who aren't exposed to pesticides.
The study -- comprised of roughly 143,000 men and women -- ran from
1982 to
2001, tracking participants' responses to extensive lifestyle
questionnaires. At the beginning of the survey, none of the
participants
showed symptoms of Parkinson's. By the end of the survey, 413
participants
had developed the disease -- an occurrence strongly linked with being
occupationally or otherwise exposed to pesticides.


The study's lead author, Alberto Ascherio of the Harvard School for
Public
Health, said, "Low-dose pesticide exposure was associated with a
significant
increase in risk for Parkinson's disease. I think this is one reason to
be
careful about using pesticides in general."


Environmental factors have long been suspected as a cause of
Parkinson's,
and Ascherio's study is the first large-scale population study to prove
the
link, though the study's design did not allow for determining how the
duration, frequency or intensity of pesticide exposure influenced
development of the disease. However, the study was able to prove that
only
pesticide exposure -- not exposure to coal dust, asbestos, exhaust,
radioactive material or formaldehyde -- correlated with developing
Parkinson's. Ascherio says the next step is figuring out specifically
what
chemicals in those pesticides cause the disease.

REPORT #2:

Northwestern University
Variations in detoxifying genes linked to Lou Gehrig's disease
Genetic variations in three enzymes that detoxify insecticides and
nerve gas agents as well as metabolize cholesterol-lowering statin
drugs may be a risk factor for developing sporadic amyotrophic lateral
sclerosis (ALS, or Lou Gehrig's disease), and possibly responsible for
a reported twofold increased risk of ALS in Gulf War veterans.

These findings, from a study led Teepu Siddique, M.D., and colleagues
at Northwestern University, open the door to investigating
gene-environment interactions as a cause of ALS and other illnesses and

to the development of molecular targets for specific treatments. The
study was published in the August 22 online issue (available now) of
the journal Neurology.


Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor,
Davee Department of Neurology and Clinical Neurosciences, professor of
cell and molecular biology and director of the Neuromuscular Disorders
Program at Northwestern University Feinberg School of Medicine.


ALS is a complex neurodegenerative disorder of the motor neurons that
results in muscle weakness, difficulty speaking, swallowing and
breathing and eventual total paralysis and death generally within five
years.


In 1993 Siddique and collaborators determined that mutations in a gene
known as SOD1 account for 20 percent of familial, or inherited, ALS (2
percent of all cases of ALS). However, the cause of sporadic ALS is
still unknown.


In earlier research Siddique and other researchers hypothesized that
sporadic ALS is modulated by variations in multiple genes interacting
with each other and environmental exposures.


The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are
located on chromosome 7q21.3, code for the production of detoxifying
enzymes involved in the metabolism of a variety of drugs,
organophosphate insecticides, such as parathion, diazinon and
chlorpyrifos, and nerve gas agents such as sarin.


Previous research described a possible twofold increased risk for
developing ALS in veterans of the Gulf War, indicating a war-related
environmental exposure to organophosphates and sarin in genetically
susceptible individuals as a possible cause. PON gene cluster variants
have previously been associated with other neurodegenerative and
vascular disorders, including Alzheimer's disease, Parkinson's disease,

coronary artery disease and stroke.


Although the Northwestern DNA study samples were not analyzed for
inclusion of Gulf War veterans, Siddique and co-researchers found
significant evidence that gene variations (polymorphisms) on the
chromosome region encompassing PON2-PON3 were strongly associated with
sporadic ALS.


"Thus, single nucleotide polymorphism genotyping in the intergenic
regions of the PON gene cluster, and replication, gene expression,
gene-gene interaction and PON serum/enzymatic studies may help
elucidate the complexity of PON cluster association with ALS," Siddique

said.


Siddique hopes to study DNA samples from Gulf War veterans with
increased incidence of sporadic ALS and has applied for their DNA from
the Veterans Administration collection.


http://www.eurekalert.org/pub_releas...-vid070506.php

I have read that the organic pesticide rotenone is a suspect for
Parkinsonšs. Easy to understand if the root was used to paralyze fish
in South America. At one time it was considered nontoxic to warm
blooded animals.

Below FYI. Note "Direct exposure of rotenone also reduced coenzyme
Q(10)" Hmmm!

Bill

PS look at this which I found in BoingBoing. Steven Hawking posting Smile)

http://answers.yahoo.com/question/;_ylt=AtjblpXOSMXPaKrJ2N9lui8jzKIX?qid=
20060704195516AAnrdOD

or http://tinyurl.com/jrrww

------------------------------------------
Complex-1 activity and (1CoolF-DOPA uptake in genetically engineered mouse
model of Parkinson's disease and the neuroprotective role of coenzyme
Q(10).

Sharma SK, El Refaey H, Ebadi M.

Department of Pharmacology, University of North Dakota School of
Medicine and Health Sciences, 501 North Columbia Road, Grand Forks, ND
58203, United States.

Regional distribution of coenzyme Q(10) and mitochondrial complex-1
activity were estimated in the brains of control-(C57BL/6),
metallothionein knock out-, metallothionein transgenic-, and homozygous
weaver mutant mice; and human dopaminergic (SK-N-SH) cells with a
primary objective to determine the neuroprotective potential of coenzyme
Q(10) in Parkinson's disease. Complex-1 activity as well as coenzyme
Q(10) were significantly higher in the cerebral cortex as compared to
the striatum in all the genotypes examined. Complex-1 activity and
coenzyme Q(10) were significantly reduced in weaver mutant mice and
metallothionein knock out mice, but were significantly increased in
metallothionein transgenic mice. The reduced complex-1 activity and
(1CoolF-DOPA uptake occurred concomitantly with negligible differences in
the coenzyme Q(10) between in the cerebral cortex and striatum of weaver
mutant mice. Administration of coenzyme Q(10) increased complex-1
activity and partially improved motoric performance in weaver mutant
mice. Direct exposure of rotenone also reduced coenzyme Q(10), complex-1
activity, and mitochondrial membrane potential in SK-N-SH cells.
Rotenone-induced down-regulation of complex-1 activity was attenuated by
coenzyme Q(10) treatment, suggesting that complex-1 may be down
regulated due to depletion of coenzyme Q(10) in the brain. Therefore,
metallothionein-induced coenzyme Q(10) synthesis may provide
neuroprotection by augmenting mitochondrial complex-1 activity in
Parkinson's disease.

PMID: 16750479 [PubMed - in process]

--
S Jersey USA Zone 5 Shade
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.
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