http://www.nutritionj.com/content/3/1/2

Co-supplementation of ferrous salts [iron] with vitamin C exacerbates
oxidative stress in the gastrointestinal tract, predisposing
individuals to ulceration, inflammatory disorders, and exacerbation of
existing chronic disorders and may cause cancer.

Iron and ascorbic acid form a potentially toxic cocktail. Ascorbic acid
has been shown to exhibit both anti-oxidant and pro-oxidant effects in
a dose related fashion. The chemical mechanisms given above have been
established demonstrating the potential for these compounds to interact
and oxidatively damage surrounding tissues. Even in healthy subjects a
positive or negative deviation from the optimal plasma ascorbic acid
level results in oxidative damage [23]. The detrimental effects of
large quantities of ascorbic acid and iron in healthy subjects and
patients with GI inflammatory diseases warrant further investigation.
In addition dietary supplements containing iron and ascorbic acid may
be deleterious as these components do not naturally come in
concentrated form (as in supplementation tablets).

http://www.stormingmedia.us/98/9806/B980632.html

Iron Deprivation Treatment of Breast Cancer: Preclinical Studies
Authors: John D. Kemp; IOWA UNIV IOWA CITY

Abstract: Further progress has been made at the pre-clinical level in
the study of iron deprivation as a potential treatment modality for
breast cancer. The MDA-MB-231 cell line appears to be resistant to
combined treatment with HES-DFO and monoclonal antibodies against the
transferrin receptor; studies with the SK- BR-3 cell line are now under

way. Preliminary data suggest that 231 cells may cease dividing but not

undergo apoptosis when acutely deprived of iron; this is in contrast to

the findings with the 38C13 lymphoma. The possibility thus arises that
distinct gene activation pathways may occur in response to iron
deprivation. New data indicate that combined treatment may produce
supra- additive increases in serum IL-6 levels and thus offer further
support for the hypothesis that enhanced macrophage activation and an
augmented acute phase response play a role in the toxicity of iron
deprivation. New data also indicate that monoclonal antibodies against
the transferrin receptor inhibit lymphocyte activation in vivo. Further

progress has been made at the pre-clinical level in the study of iron
deprivation as a potential treatment modality for breast cancer. The
MDA-MB-231 cell line appears to be resistant to combined treatment with

HES-DFO and monoclonal antibodies against the transferrin receptor;
studies with the SK- BR-3 cell line are now under way. Preliminary data

suggest that 231 cells may cease dividing but not undergo apoptosis
when acutely deprived of iron; this is in contrast to the findings with

the 38C13 lymphoma. The possibility thus arises that distinct gene
activation pathways may occur in response to iron deprivation. New data

indicate that combined treatment may produce supra- additive increases
in serum IL-6 levels and thus offer further support for the hypothesis
that enhanced macrophage activation and an augmented acute phase
response play a role in the toxicity of iron deprivation. New data also

indicate that monoclonal antibodies against the transferrin receptor
inhibit lymphocyte activation in vivo.

Limitations: APPROVED FOR PUBLIC RELEASE
Description: Annual rept. 23 Dec 96-22 Dec 97
Pages:  27
Report Date: FEB 1998
Report number:  B980632
Keywords relating to this report:
ACTIVATION
BREAST CANCER
CELLS(BIOLOGY)
CLINICAL MEDICINE
CONTRAST
DEPRIVATION
GENES
HYPOTHESES
IN VIVO ANALYSIS
IRON
LYMPHOCYTES
MACROPHAGES
MONOCLONAL ANTIBODIES
NEOPLASMS
RESPONSE
RESPONSE(BIOLOGY)
TOXICITY

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Tom

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