On Jun 13, 5:06 pm, Taka <taka0... at (no spam) gmail.com> wrote:

On Jun 13, 9:33 pm, MattLB <mat... at (no spam) angelfire.com> wrote:
Mentioning sugar is a
complete red herring.

Yet VitC is made from sugar,

So are many other molecules that also don't have the metabolic
consequences of high sugar levels.

enters cells via the same receptors as
sugar and its absorption is competitively inhibited by sugar ...

All of which has nothing to do with what happens when they get inside
the cells.

Any molecule that can become a free radical
through interaction with iron will have the same effect.

Like our wonderful PUFAs. BTW you forgot oxygen without which iron is
powerless.

Not true. Iron can react with lipid hydroperoxides and others without
the presence of oxygen.

The combination O2+Fe+VitC+PUFAs is the best setting for
getting full spectrum of lipid hydroperoxides and free radicals and
you can even get so called AGEs if you throw in sugars.

Something sugars and vit C don't have in common you mean.

I have mentioned previously how sugar and saturated fatty acids (which
are rare in their free form in the body BTW)

Only when insulin levels are high. At other times, especially on low
carb diets, levels of free FA are high.

MattLB

"Taka" <taka0... at (no spam) gmail.com> wrote in message

news:9b4f0d67-dc25-4f26-9a71-1f9b93edeed6 at (no spam) a1g2000hsb.googlegroups.com...

Small/appropriate VitC amount at the right place is good and essential
for e.g. collagen synthesis. Large amount at the wrong place may be
dangerous depending on the presence of Fe, PUFAs and the like. AFAIK
there are fewer studies, if any, showing a proinflammatory properties
of VitE. VitE protects from lipid peroxides while VitC may facilitate
their formation. Since lipid peroxides are proapoptotic and activate
p53 high doses of VitC are used intravenously to kill cancers. The
genotoxicity of VitC was refuted later by an artificial system in
vitro experiment which I wouldn't trust as much as the original
Science paper:

Well, the first cite I found in my boy scout googling "shows" that alpha
tocopherol all by its lonesome forms lipid peroxides. They even show a
mechanism. Vit C stops this.
So your "if any" remark is immediately refuted--apparently you did not
bother to read my cite.
Do you think this is the *only* cite of its kind, regarding Vit E?? Did I
get lucky?
iirc, I think even some of *your cites* discussed Vit E in this regard.

And on what authority do you "trust" one study over another? Do you have
personal laboratory experience in the field, or have you compiled citations
of these articles, for putative credibility?

And, how does one selectively deliver Vit C "to the right places"??





Science 15 June 2001:
Vol. 292. no. 5524, pp. 2083 - 2086
DOI: 10.1126/science.1059501

Vitamin C-Induced Decomposition of Lipid Hydroperoxides to Endogenous
Genotoxins

Seon Hwa Lee, Tomoyuki Oe, Ian A. Blair*

Epidemiological data suggest that dietary antioxidants play a
protective role against cancer. This has led to the proposal that
dietary supplementation with antioxidants such as vitamin C (vit C)
may be useful in disease prevention. However, vit C has proved to be
ineffective in cancer chemoprevention studies. In addition, concerns
have been raised over potentially deleterious transition metal ion-
mediated pro-oxidant effects. We have now determined that vit C
induces lipid hydroperoxide decomposition to the DNA-reactive
bifunctional electrophiles 4-oxo-2-nonenal, 4,5-epoxy-2(E)-decenal,
and 4-hydroxy-2-nonenal. The compound 4,5-Epoxy-2(E)-decenal is a
precursor of etheno-2'-deoxyadenosine, a highly mutagenic lesion
found
in human DNA. Vitamin C-mediated formation of genotoxins from lipid
hydroperoxides in the absence of transition metal ions could help
explain its lack of efficacy as a cancer chemoprevention agent.

For you "Boy Scout chemists", do you have any idea what the transition
metal ion-
mediated pro-oxidant effects are? This is different from the PLA2
induction

Boy-scout chemist or not, I know that acid lowers pH, hot water raises temp,
and reducing agents reduce, they don't oxidize.

"transition metal ion mediated pro-oxidant effect" is self-explanatory.
Since you seem to be the expert, why don't you discuss the *mechanisms* by
which these ions oxidize? Or peroxidize? I would be genuinely interested
in a coherent explanation.

For example, Fe3+ is more of an oxidant than Fe2+, by definition. Which
suggests, btw, that FeSO4 is a "safer" source of iron than FeCl3.
Vit C is famous for reducing Fe3+ to Fe2+. So how can this be *pro
oxidizing*?? Fe2+ may still be oxidizing, but markedly less than Fe3+

I can think of only one way Fe2+ could be made more oxidizing than Fe3+:

There may be an enzyme that has a greater binding constant for Fe2+ than for
Fe3+. If this Fe2+(enzyme) complex is in fact the culprit in an oxidizing
or peroxidizing (pro-inflammatory?) process, then indeed Vit C would be
increasing pro-oxidation in this specific context.

Which is not likely, because afaik, transition metals are buried inside
enzymes (metallo enzymes), and I don't recall ions often binding to enzymes
at active sites, for obvious reasons of poor regulatory control by
ubiquitously available ions.

Mg2+ stabilizing ATP is of course a different story.

And, you would be obligated to show that this transition metal ion-enzyme
complex exists. You, or one of those studies, referred to VitC-Fe complex;
I doubt if such a thing exists, just as intact FeCl3 in solution does not
exist.

Transition metal complexes *do* in fact exist, strictly in the form of
coordination compounds, such as Cr(nicotinate)3. But this has nothing to do
with oxidation or reduction, but rather simple transport of Cr3+.

Please cite mechanisms, if you are able to. These are much more informative
and convincing than dart-thrown abstracts.
--
DT

On Jun 17, 12:16 am, MattLB <mat... at (no spam) angelfire.com> wrote:
On Jun 13, 5:06 pm, Taka <taka0... at (no spam) gmail.com> wrote:
Like our wonderful PUFAs. BTW you forgot oxygen without which iron is
powerless.

Not true. Iron can react with lipid hydroperoxides and others without
the presence of oxygen.

Without oxygen, 1 molecule Fe can oxidize 1 molecule PUFA but if
oxygen is present 1 molecule of Fe can catalyze the oxidation of
thousands of PUFA molecules (of course if you have thousands of O2
molecules).

Well I guess VitC can produce AGEs as well, but most of them are
derived from PUFAs anyway.

I have mentioned previously how sugar and saturated fatty acids (which
are rare in their free form in the body BTW)

Only when insulin levels are high. At other times, especially on low
carb diets, levels of free FA are high.

Never heard of that, triglycerides yes but free FAs floating in the
blood? Perhaps you mean chylomicrons?

Anyway MattLB, to contribute to this thread in a constructive way tell
us what is your idea of the molecular mechanism by which VitC enhances
immunity and fights infections in the body?

Anyway MattLB, to contribute to this thread in a constructive way tell
us what is your idea of the molecular mechanism by which VitC enhances
immunity and fights infections in the body?

That's not what the thread's about so it would be veering off the
topic, even if I had a quick answer for you, which I don't.