Hi!
I read with interest your article on NADH. There is one slight
misinterprettion about NADH. NADH stands for Nicotinamide Adenine
Dinucleotide-Reduced (H stands for Reduced; when it isoxiized by
NADH-dehydrogenase (part of mitochondrial complex I) it becomes NAD
(oxidized by the removal of H atom. Complex 1 of the mammalian electron
transfer chain is composed of at lest 43protein subunits. It catalyzes the
transfer of electrons from NADH (Reduced Nicotinamide Adenine Dinucleotide)
to ubiquinone (Co E Q 10) and translocates protons from the
mitochondrialmatrix to the
intermembrane space.
PD is also asscoiated with a systemic defect in this mitochondrial complex 1
activity. Animal models indicate that exposure to inhibitors of
mitochondrial complex 1, (such as rotenone and MPTP) including pesticides,
is sufficient to produce the features of PD. But, the genetic factors
clearly modulate the susceptibility. Complex 1 defects may result in
oxidative stress and increase the susceptibility of neurons to excitotoxic
death. In this way, environmental exposures and mitochondrial dysfunction
may interact and result in neurodegenration by destroying dopaminergic
neurons.
I wonder then, NADH in conjunction with Co E Q10 may be even more beneficial
than both taken individually!
I also ran into a very good reference for us to read:
Kidd, PM. Parkinson's disease as multifactorial oxidative neurodegeneration:
Implications for integrative management.Altern Med Review 2000. 5: 502529.
Raj
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From: "Meadow Creek Ranch / Schaaf Angus" <[log in to unmask]>
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Sent: Tuesday, January 21, 2003 11:05 AM
Subject: Re: NADH
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