Vitamin C, tumor food

From: Ian Goddard (
Date: Sun Apr 23 2000 - 21:49:28 MDT

About the following study, Science News (10/2/99) states:
"Leukemia cells, prostate tumors, and breast cancers are
among malignancies that like to stock up on copious amounts
of ascorbate, also known as vitamin C, a new study finds."
Perhaps tumor cells might use vitamin C to defend themselves
against attacks from the immune system, which I understand
generates free radicals to destroy pathogens, and probably
cancer. Important for life-extenders to note, the study
found that the co-administration of superoxide dismutase
(SOD) with vitamin C prevented the uptake of vitamin C by
tumor cells, for reasons that are indicated (keep in mind
if you want to take SOD pills that Durk Pearson and Sandy
Shaw state in "Life Extension" that "one part in 10,000
of SOD administered orally survives processing in the
stomach and receaches the bloodstream." page 496):


Cancer Research, 1999 Sep 15;59(18):4555-8

Stromal cell oxidation: a mechanism by which
tumors obtain vitamin C.

Agus DB, Vera JC, Golde DW

Department of Medicine, Memorial Sloan-Kettering
Cancer Center, New York, New York 10021, USA.

Human tumors may contain high concentrations of
ascorbic acid, but little is known about how they
acquire the vitamin. Certain specialized cells can
transport ascorbic acid directly through a sodium
ascorbate cotransporter, but in most cells, vitamin
C enters through the facilitative glucose transporters
(GLUTs) in the form of dehydroascorbic acid, which
is then reduced intracellularly and retained as
ascorbic acid. Mice with established hematopoietic
and epithelial cell xenografts wereascorbic acid.
Most hematopoietic and epithelial tumor cell lines
can only transport vitamin C in the oxidized form
(dehydroascorbic acid) in vitro; however, when grown
as xenografts in mice, they rapidly accumulated
vitamin C after administration of radiolabeled
ascorbic acid. The involvement of the GLUTs in
vitamin C uptake by the xenografted tumors was
demonstrated by competitive inhibition with D-glucose
but not L-glucose. Because the malignant cells were
not capable of directly transporting ascorbic acid,
we reasoned that the ascorbic acid was oxidized to
dehydroascorbic acid in the tumor microenvironment.
Tumor accumulation of vitamin C in animals injected
with ascorbic acid was inhibited by coadministration
of superoxide dismutase, implying a role for superoxide
anion in the oxidation of ascorbic acid. Whereas the
epithelial cancer cell lines could not generate
superoxide anion in culture, the minced xenograft
tumors did. Our studies show the transport of
dehydroascorbic acid by GLUTs is a means by which
tumors acquire vitamin C and indicate the oxidation
of ascorbic acid by superoxide anion produced by
cells in the tumor stroma as a mechanism for
generating the transportable form of the vitamin.


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