Have you read the evidence I posted in the general forum, in the thread entitled: Glycation's role in "disease" and "aging." ?
There is one study that is particularly good:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of April
26, pp. 9982-9986, 1996
© 1996 by The American Society for Biochemistry and Molecular Biology,
Inc. Printed in U.S.A.
"The Advanced Glycation End Product, Ne-(Carboxymethyl)lysine, Is
a Product of both Lipid Peroxidation and Glycoxidation Reactions*"
QUOTE: "CML is also formed during
metal-catalyzed oxidation of polyunsaturated fatty
acids in the presence of protein... We also report that CML, heretofore
described as a gly-coxidation
product, is formed during peroxidation of polyunsat-urated
fatty acids (PUFA) in the presence of ribonuclease A (RNase), a protein
that contains neither enzymatically nor
nonenzymatically attached carbohydrate... oxidation of fatty acid is
clearly a more efficient source of CML, despite the fact that the
glucose is in solution throughout the course of the experiment,
while the PUFA are only progressively solubilized. Further,
after 6 days of incubation, a large fraction of the arachidonate
was oxidized based on its solubilization in the aqueous phase,
while 2% of the glucose is oxidized during this same time
period... The observations described above indicate that CML,
previ-ously
described as a glycoxidation product or AGE, may, in fact,
be derived from PUFA during lipid peroxidation reactions. UNQUOTE. |
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