Med Hypotheses 2001 Nov;57(5):539-43
The possible crucial role of iron accumulation combined with low
tryptophan, zinc and manganese in carcinogenesis.
Johnson S.
Iron can react with citric acid, interfering with the Krebs cycle,
hence
with oxidative phosphorylation. Free iron (Fe) can cause considerable
oxidative damage both through Fenton reactions and by activating
xanthine oxidase, which produces both superoxide (O(2-)) and uric
acid
(abundant in many cancers). It can also react with lactic acid,
reducing
its elimination and increasing the acidity of the cytoplasm. Fe can
also
wreak havoc by reacting with tryptophan, the least abundant and most
delicate essential amino acid, which is necessary for the production
of
serotonin and other substances required by the immune system to fight
cancer. On the other hand, in the presence of iron, the tryptophan
metabolite quinolinate causes intense lipid peroxidation. Similarly,
several other carcinogenic metabolites of tryptophan are particularly
dangerous in the presence of Fe. Excess Fe may also interfere with
manganese superoxide dismutase and impair the initiation of apoptosis
by
the mitochondrion, rendering the cells impervious to all the signals
to
undergo apoptosis from without and from within the cell. Moreover, Fe
may also play a crucial role on telomere repair, by activating
telomerase. Therefore, by inhibiting apoptosis and enhancing
chromosome
repair, Fe may bestow immortality upon the cancer cell. Furthermore,
Fe
is one of the triggers for mitosis. Therefore, increased Fe levels
may
be essential for the rapid growth characteristic of many
malignancies.
In turn, the rapid growth further depletes resources from the healthy
tissues, exacerbating the deficiencies of the other elements and
reducing the ability to fight the malignancy.
Copyright 2001 Harcourt
Publishers Ltd.
PMID: 11735307 [PubMed - indexed for MEDLINE]
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ferrous@paris.com - 27 Sep 2007 15:37 GMT
"Free iron (Fe) can cause considerable oxidative damage"
What are the two major ways the body regulates free iron?
Jesus ate a mediterranean diet.
ironjustice - 27 Sep 2007 15:51 GMT
>> On Sep 27, 7:37 am, ferr...@paris.com wrote:
"Free iron (Fe) can cause considerable oxidative damage"
What are the two major ways the body regulates free iron?
<<
You mean .. labile iron pool .. ? .. is that what you mean ..
Let's see ..
Let's type that in .. and see .. ?
That would be the easy thing to do ..
Short pause here to make it appear as if I really looked this up ...
--
--
Sooo .. free iron / labile iron pool .. is "unregulated iron" ..
I guess if it is .. unregulated .. means the body does NOT .. regulate
it .. ?
Yep ..
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Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
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ferrous@paris.com - 27 Sep 2007 17:31 GMT
>> Free iron (Fe) can cause considerable oxidative damage"
> What are the two major ways the body regulates free iron?
How about this?
[_] 1: World J Gastroenterol. 2007 Sep 21;13(35):4737-45. Liver-gut
axis in the regulation of iron homeostasis.
The human body requires about 1-2 mg of iron per day for its
normal functioning, and dietary iron is the only source for
this essential metal. Since humans do not possess a mechanism
for the active excretion of iron, the amount of iron in the
body is determined by the amount absorbed across the proximal
small intestine and, consequently, intestinal iron absorption
is a highly regulated process. In recent years, the liver has
emerged as a central regulator of both iron absorption and
iron
release from other tissues. It achieves this by secreting a
peptide hormone called hepcidin that acts on the small
intestinal epithelium and other cells to limit iron delivery
to
the plasma. Hepcidin itself is regulated in response to
various
systemic stimuli including variations in body iron stores, the
rate of erythropoiesis, inflammation and hypoxia, the same
stimuli that have been known for many years to modulate iron
absorption. This review will summarize recent findings on the
role played by the liver and hepcidin in the regulation of
body
iron absorption.
PMID: 17729395 [PubMed - in process]