Hi olsen!!!
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-ANSWER-
I will start with some short definitions:
What is an enzyme?
It is a protein that speeds up chemical reactions in the body.
From Wikipedia I summed up the following:
"An enzyme is a protein, or protein complex, that catalyzes a chemical
reaction in an organism. Within biological cells many chemical
reactions occur, but without enzymes they would happen too slowly to
sustain life. Enzymes speed up reactions by a factor of one thousand
times or more..."
http://en.wikipedia.org/wiki/Enzyme
What is a coenzyme?
It is an organic non-protein molecule, a small organic molecule that
binds to an enzyme and is required for its catalytic activity. It is
also called cofactor. It is not a protein but sometimes is a vitamin.
Joining this two definitions we can say that the enzymes are
substances required to make possible or accelerate chemical reactions
in a living organism. Note that the enzymes are not used up or changed
during such chemical reactions. In general enzymes require minerals
(for example magnesium or zinc), and/or a non-protein organic
chemicals, called a coenzymes. Examples of coenzymes are vitamin B6,
vitamin B12, folic acid, and Coenzyme Q10.
-The Coenzyme Q10 (CoQ10):
Coenzyme Q are any of several quinones that function as
electron-carrying coenzymes. CoQ10 is involved in the synthesis of
adenosine triphosphate (ATP), the body's primary source of
intracellular energy.
Again at Wikipedia I found the following:
"Coenzyme Q (CoQ), also known as ubiquinone or ubiquinol, is a
biologically active quinone with an isoprenoid side chain, related in
structure to vitamin K and vitamin E...
The various kinds of Coenzyme Q can be distinguished by the number of
isoprenoid side chains they have. The most common CoQ in human
mitochondria is Q10...
CoQ is found in the membrane of the mitochondrion...
Because of its ability to transfer electrons and therefore act as an
antioxidant, Coenzyme Q has become a fashionable dietary
supplement..."
http://en.wikipedia.org/wiki/Coenzyme_Q
-Mitochondrion:
"In cell biology, a mitochondrion is an organelle found in the cells
of most eukaryotes. Mitochondria are sometimes described as "cellular
power plants" because their primary purpose is to manufacture
adenosine triphosphate (ATP), which is used as a source of energy...:
Mitochondria convert the potential energy of food molecules into ATP..."
From "Mitochondrion - Wikipedia, the free encyclopedia":
http://en.wikipedia.org/wiki/Mitochondrion
-Adenosine triphosphate (ATP):
Enzymes in chemiosmotic synthesis are arranged in an electron
transport chain that is embedded in a membrane. In eukaryotes this
membrane is in either the chloroplast or mitochondrion.
"Adenosine triphosphate (ATP), the energy currency or coin of the
cell, transfers energy from chemical bonds to endergonic (energy
absorbing) reactions within the cell. Structurally, ATP consists of
the adenine nucleotide plus two other phosphate groups...
Energy is stored in the covalent bonds between phosphates, with the
greatest amount of energy (approximately 7 kcal/mole) in the bond
between the second and third phosphate groups. This covalent bond is
known as a pyrophosphate bond.
We can write the chemical reaction for the formation of ATP as:
a)in chemicalese:
ADP + Pi + energy ----> ATP
b)in English:
Adenosine diphosphate + inorganic Phosphate + energy produces
Adenosine Triphosphate
The chemical formula for the expenditure/release of ATP energy can be written as:
a)in chemicalese:
ATP ----> ADP + energy + Pi
b)in English:
Adenosine Triphosphate produces Adenosine diphosphate + energy +
inorganic Phosphate
An analogy between ATP and rechargeable batteries is appropriate. The
batteries are used, giving up their potential energy until it has all
been converted into kinetic energy and heat/unusable energy. Recharged
batteries (into which energy has been put) can be used only after the
input of additional energy. Thus, ATP is the higher energy form (the
recharged battery) while ADP is the lower energy form (the used
battery). When the terminal (third) phosphate is cut loose, ATP
becomes ADP (Adenosine diphosphate; di= two), and the stored energy is
released for some biological process to utilize. The input of
additional energy (plus a phosphate group) "recharges" ADP into ATP
(as in my analogy the spent batteries are recharged by the input of
additional energy)..."
From "ATP AND BIOLOGICAL ENERGY"
http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookATP.html
-Role of CoQ10 in mitochondrial ATP synthesis:
As we said the most common CoQ in human mitochondria is CoQ10 and it
is found in the membrane of the mitochondrion.
Another important fact is that the enzymes in ATP synthesis are
arranged in an electron transport chain that is embedded in a
mithocondrial membrane. Strongly related to this, the ability of the
coenzyme Q to accept and donate electrons is a critical feature in ATP
synthesis and make the CoQ10 an essential cofactor of this process.
"The conversion of energy from carbohydrates and fats to adenosine
triposphate (ATP), the form of energy used by cells, requires the
presence of coenzyme Q in the inner mitochondrial membrane. As part of
the mitochondrial electron transport chain, coenzyme Q accepts
electrons from reducing equivalents generated during fatty acid and
glucose metabolism and transfers them to electron acceptors. At the
same time, coenzyme Q transfers protons outside the inner
mitochondrial membrane, creating a proton gradient across that
membrane. The energy released when the protons flow back into the
mitochondrial interior is used to form ATP"
From "Coenzyme Q10, Linus Pauling Institute's Micronutrient Information Center":
http://lpi.oregonstate.edu/infocenter/othernuts/coq10/
-Coenzyme Q10 and Parkinson's disease:
Parkinson's disease (PD) is a disorder caused by a highly selective
death of cells in a small part of the brain called the substantia
nigra. Neurons that produce dopamine die in this part of the brain
that coordinates movement. This causes a gradual loss of these cells
which causes PD symptoms. Because Parkinson's disease is a progressive
disorder, these symptoms become worse with time.
The Flow of Electrons in the synthesis of ATP shows the importance of CoQ10:
·NADH oxidized by CoQ at complex I
·FADH2 oxidized by CoQ at complex II
·CoQ oxidized by cytochrome c at complex III
·Cytochrome c oxidized by O2 at complex IV
See at the following document the diagram of "Flow of Electrons" at
page 17 of the document:
"Electron Transport and Oxidative Oxidative Phosphorylation Phosphorylation":
http://web.indstate.edu/thcme/mwking/oxidativephosphorylation.pdf
·Why patients with Parkinson's disease lost dopamine-producing nerve
cells in the substantia nigra, a part of the mid-brain's grey matter?
Several researches have shown that a reduction of the activity at a
certain step in mitochondrial energy production, called Complex I, the
first complex of the electron transfer chain of mitochondria or
cellular respiratory chain, causes an increase in the number of oxygen
free radicals, which are known to be toxic to cells, such as those in
the substantia nigra.
Clifford Shults, M.D. and Richard Haas, M.D., in the UCSD Department
of Neurosciences, began a series of experiments that shown the
activity of complex I was significantly lower in the Parkinsonian
patients. Then, knowing the importance of the CoQ10 in the cells
respiration process, they found that the levels of coenzyme Q10 in the
platelet mitochondria are significantly lower in Parkinsonian
patients. So we have that in patients with Parkinson's disease
mitochondrial function is impaired and coenzyme Q10 levels are
reduced.
The researchers' next step was to see if the increment of the levels
of CoQ10 could stop or revert the Parkinson's disease symptoms.
"Humans can make CoQ10 or we can absorb it from our food. However, we
cannot manufacture CoQ10 from simple nutrients or CoQ10?s building
blocks. As we age, many of us lose our ability to efficiently make
CoQ10. Thus, many persons will depend on their food for all of their
CoQ10, and therefore it becomes a vitamin to those individuals. To
make matters worse, foods lose coenzyme Q?s (CoQ1 to CoQ10) with
processing and storage.
Coenzymes are not inactivated by stomach acids and are readily
absorbed. When CoQ10 is taken orally, it is incorporated into the
mitochondria of cells throughout the body where it facilitates and
regulates the oxidation of fats and sugars into energy....
In a report published in the Annals of Neurology (August 1997), a new
mechanism was identified that showed that CoQ10 might be effective in
the prevention and treatment of Parkinson?s disease.
This study showed that the brain cells of Parkinson?s patients have a
specific impairment that causes the disruption of healthy
mitochondrial function. It is known that "mitochondrial disorder"
causes cells in the substantia nigra region of the brain to
malfunction and die, thus creating a shortage of dopamine.
An interesting finding was that CoQ10 levels in Parkinson?s patients
were 35% lower than age-matched controls. This deficit of CoQ10 caused
a significant reduction in the activity of enzyme complexes that are
critical to the mitochondrial function of the brain cells affected by
Parkinson?s disease.
The ramifications of this study are significant. Parkinson?s disease
is becoming more prevalent as the human life span increases. The new
study confirms previous studies that Parkinson?s disease may be
related to CoQ10 dificiency. The conclusion of the scientists:
'The causes of Parkinson?s disease are unknown. Evidence suggests that
mitochondrial dysfunction and oxygen free radicals may be involved in
its pathogenesis. The dual function of CoQ10 as a constituent of the
mitochondrial electron transport chain and a potent antioxidant
suggest that it has the potential to slow the progression of
Parkinson?s disease'."
Text between quotes was summarized from "Coenzyme Q10":
http://www.road-to-health.com/am/publish/printer_38.shtml
We have that Parkinson's disease patients show lower levels of CoQ10,
and this is related to the reduction activity of the Complex I in the
mithocondrial membrane of the cells of the sustantia nigra, this
results in an increase of the number of oxygen free radicals in this
region of the brain and promote the dead of the neurons that produce
dopamine. Oral administration of CoQ10 increase the level of CoQ10
restoring the activity of the Complex I and by this slow the
progression of Parkinson's disease, specially in early states.
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For additional reference I suggest you to read the following pages and documents:
"COENZYME Q10 SLOWS PROGRESSION OF EARLY PARKINSON?S DISEASE":
http://www.neurologyreviews.com/dec02/nr_dec02_coenzymeq10.html
"Coenzyme Q10 Summary of References":
http://faculty.washington.edu/~ely/coenzq10abs.html
"Study Suggests Coenzyme Q10 Slows Functional Decline in Parkinson's Disease":
http://www.ninds.nih.gov/news_and_events/pressrelease_parkinsons_coenzymeq10_101402.htm
"Co Q10 -Mechanisms of Action and more":
http://www.annieappleseedproject.org/coq10morfrom.html
"Alternative Medicine Review: Ubiquinone and mitochondria in oxidative
stress of Parkinson's disease - coenzyme q10 - Abstract":
http://www.findarticles.com/p/articles/mi_m0FDN/is_4_6/ai_78539449
"Serum levels of coenzyme Q in patients with Lewy body disease":
This document is indirectely related to Parkinson's disease, but it
will give you useful info about CoQ10 chemical activity in the body.
http://www.risolidaria.org/canales/canal_envejecimiento/pdf/JNT.pdf
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Search strategy:
coenzyme definition
q10 parkinson's
q10 atp synthesis
q10 atp synthesis parkinson
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I hope that this helps you. Feel free to request for any clarification
needed before rate this answer.
Best regards.
livioflores-ga |
Clarification of Answer by
livioflores-ga
on
24 Aug 2004 21:38 PDT
Hi olsen!!
Related to your request of clarification this is what I found:
"A possible role of coenzyme Q10 in the etiology and treatment of
Parkinson's disease." by Shults CW, Haas RH, Beal MF.
BioFactors
Issue: Volume 9, Numbers 2-4 / 1999
Pages: 267 - 272
Abstract:
"Parkinson's disease (PD) is a degenerative neurological disorder.
Recent studies have demonstrated reduced activity of complex I of the
electron transport chain in brain and platelets from patients with PD.
Platelet mitochondria from parkinsonian patients were found to have
lower levels of coenzyme Q10 (CoQ10) than mitochondria from
age/sex-matched controls. There was a strong correlation between the
levels of CoQ10 and the activities of complexes I and II/III. Oral
CoQ10 was found to protect the nigrostriatal dopaminergic system in
one-year-old mice treated with MPTP, a toxin injurious to the
nigrostriatal dopaminergic system. We further found that oral CoQ10
was well absorbed in parkinsonian patients and caused a trend toward
increased complex I activity. These data suggest that CoQ10 may play a
role in cellular dysfunction found in PD and may be a potential
protective agent for parkinsonian patients."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10416040&itool=iconabstr
You can gain access to the full text article for a fee.The price for
this article is $17.00:
http://iospress.metapress.com/app/home/contribution.asp?wasp=af8lvmmxqh0ujekged4t&referrer=parent&backto=issue,23,38;journal,20,30;linkingpublicationresults,1:103144,1
------------------------------------------------------------
"Coenzyme Q10 levels correlate with the activities of complexes I and
II/III in mitochondria from parkinsonian and nonparkinsonian
subjects." by Shults CW, Haas RH, Passov D, Beal MF.
Annals of Neurology
1997 Aug;
Volume: 42
Issue: 2
Pages: 261-4.
Abstract:
"The activities of complex I and complex II/III in platelet
mitochondria are reduced in patients with early, untreated Parkinson's
disease. Coenzyme Q10 is the electron acceptor for complex I and
complex II. We found that the level of coenzyme Q10 was significantly
lower in mitochondria from parkinsonian patients than in mitochondria
from age- and sex-matched control subjects and that the levels of
coenzyme Q10 and the activities of complex I and complex II/III were
significantly correlated."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9266740&itool=iconabstr
"Low platelet mitochondrial complex I and complex II/III activity in
early untreated Parkinson's disease." by Haas RH, Nasirian F, Nakano
K, Ward D, Pay M, Hill R, Shults CW.
Annals of Neurology
1995 Jun;
Volume: 37
Issue: 6
Pages: 714-22
Abstract:
"Following the discovery of inhibition of electron transport complex 1
by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP),
which produces a parkinsonian syndrome in humans, monkeys, and mice,
several laboratories have reported abnormalities of complex I and
other electron transport complexes (ETCs) in various tissues from
patients with Parkinson's disease (PD). Criticism of the significance
of these findings in the etiology of PD has centered on whether drug
treatments or the debilitation of the disease process itself produced
the low ETC activities. We present results from a blinded study of
platelet mitochondrial ETC activities in 18 early untreated PD
patients and 18 age- and sex-matched controls and in 13 spousal
controls. Lower complex I activity in platelet mitochondria of PD
patients was seen in early untreated disease and thus cannot be due to
debilitation or drug therapy. Home environmental factors seem an
unlikely explanation for the reduced complex I activity in PD patients
but have not been excluded. Complex II/III activity was also reduced
by 20% in PD compared with age-/sex-matched controls. The low complex
I and II/III activities in platelet mitochondria appear to be related
to the etiology of PD."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7778844&itool=iconabstr
Unfortunately there I cannot find online access to these two last
interesting articles, but I think that you have all the necessary info
to find them in a library near your location.
Some libraries offers online catalogs, so if you let me know in which
city you live, I will gladly help you to find an accessible library
that has these articles available to read.
-----------------------------------------------------
I also posted in the main answer a link to the abstrac of this interesting article:
"Ubiquinone (Coenzyme Q10) and Mitochondria in Oxidative Stress of
Parkinson's Disease" by M. Ebadi, P. Govitrapong, S. Sharma, D.
Muralikrishnan, S. Shavali, L. Pellett, R. Schafer, C. Albano, Josh
Eken
·Biological Signals and Receptors·
Vol. 10,
No. 3-4,
May?August 2001
Pages: 224-253.
http://www.findarticles.com/p/articles/mi_m0FDN/is_4_6/ai_78539449
You can gain access to the full text article for a fee ($35.00)
through the following page:
http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=bsi10224
I also suggest you to visit the page of this volume titled:
"Oxidative Stress in Mitochondria Disorders of Aging"
Vol. 10, No. 3-4, 2001
May?August 2001
ISBN 3-8055-7236-0
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=Ausgabe&ProduktNr=224154&Ausgabe=226821
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I hope that this helps you. Feel free to request for further
assistance if it is needed.
Best regards.
livioflores-ga
|
