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Excerpts
from the Annual Meeting for Experimental Biology New
Research Confirms That Aged Garlic Extract with its Various Constituents
May Be a Prudent Addition to Anyone's Diet as it May Help to Maintain the Health
of Various Organs AGE
for a Healthy Prostate Dr.
John Pinto and his team of researchers at Memorial Sloan Kettering Cancer Center
in New York found that S-allylmercaptocysteine (SAMC), a constituent in Aged
Garlic Extract (AGE) developed through the aging process, may inhibit the growth
of human prostate cancer cells (1). Exposing
these cells to the male hormone testosterone causes them to grow at a faster
rate. SAMC was found to enhance the degradation of cellular testosterone
two-fold and to slow cancer cell growth by as much as 70% (2). Therefore, these
researchers suggested that SAMC, by breaking down cellular testosterone,
hampered the progression or activation of these cancer cells.
According to Dr. Richard Rivlin, Sloan Kettering's director of clinical
nutrition, these cultured cells also produce compounds characteristic of human
prostate tumors, making them a good model of human disease.
Specifically,
prostate specific antigen (PSA) is released from these cancer cells when they
are growing and is used as a marker of cancer progression in men.
PSA itself can also promote cancer cell proliferation.
Treatment with SAMC also markedly reduced PSA levels. AGE
for a Healthy Colon Dr.
John Milner and his group at Pennsylvania State University found that both SAMC
and diallyl disulfide (DADS), another constituent in AGE, are effective at
suppressing the growth of cultured human colon tumor cells (3). At equimolar
amounts, DADS was most effective. Twenty-five
mcg of DADS and 300 mcg of SAMC caused a 23% suppression in cell growth.
DADS also assisted the conversion of these cancer cells from a mutated to
a normal state (from G1 to S phase). Many
factors are involved in the development and progression of colon cancer and AGE
alone will likely not prevent cancer. However,
continuous intake may provide beneficial compounds the colon can use as
ammunition against abnormal cell growth. AGE
Suppresses Enzyme Systems in the Body That Generate Toxins Dr.
John Milner and his team at Pennsylvania State University used a biochemical
model to determine if Kyolic and/or one of its minor constituents, DADS, could
inhibit cellular enzyme systems, which generate toxins from pre-cancerous
chemicals (4). Specifically, they tested the cytochrome P450 system,
particularly CYP 2E1activity. This enzyme system is enhanced by ethanol and it
is at least partially responsible for converting precancerous compounds into
cancerous compounds. Blocking this
enzyme system can hamper the generation of some carcinogens. Since CYP 2E1 is
also capable of converting chlorzoxazone (CZX, a muscle relaxer) into its
metabolite 6-OH hydroxychlorzoxazone (6-OHCZX), measurement of 6-OHCZX in the
urine can be used to determine CYP 2E1activity.
Rats were given Kyolic and DADS for two weeks, at the end of which time
they were then given CZX. Over the
following 24 hours, excretion of 6-OHCZX was measured.
Values for 6-OHCZX were reduced 15% in Kyolic treated rats and 27% in
DADS-treated rats, thus demonstrating that Kyolic and its constituent DADS
suppress CYP 2E1 activity. The researchers concluded that since Kyolic contains
only a small amount of DADS, other compounds present in Kyolic, such as S-allyl
cysteine (SAC), must have an ability to suppress CYP 2E1 activity.
This conclusion was based on former research in which SAC was found to
inhibit both the formation and bioactivation of the liver carcinogen
nitrosomorpholine (NMOR) (5). Adding SAC to a solution of sodium nitrite and
morpholine prevented these two compounds from generating the carcinogen
nitrosomorpholine. Once generated, SAC also prevented NMOR's ability to mutate a
cell model. Therefore, SAC
prevented both the generation of this carcinogen and its damaging effects. AGE
Demonstrates Antioxidant Activity The
antioxidative effects of AGE may help to maintain healthy function of the
cardiovascular system by quenching free radicals, which cause damage to the
lining of veins and arteries. Damage to cells lining the veins and arteries can
lead to scarring that may eventually block blood flow as cholesterol, platelets,
immune cells and smooth muscle cells accumulate over the damaged area.
Dr. Lau and his team from Loma Linda University found that AGE protected
vascular endothelial cells (specific cells which line the veins and arteries)
from direct oxidative damage (6). In
this study, AGE enhanced antioxidative enzyme systems within these cells that
quench free radicals and prevented them from causing damage.
Specifically, AGE enhanced two enzyme systems, the glutathione (GSH)
redox cycle and superoxide dismutase (SOD) activity. SOD
quenches the potent, damaging superoxide radical and glutathione quenches an
array of oxidants known to cause damage. AGE
demonstrated further antioxidant activity by scavenging hydrogen peroxide.
Hydrogen peroxide yields a free radical by reacting with iron or copper (called
the Fenton reaction). The resulting free radical damages both membranes and DNA
and/or induces lipid peroxidation (damage to lipids or fats in cell membranes).
Nagatoshi Ide and other researchers from Japan recently found that by scavenging
or quenching hydrogen peroxide, AGE and its constituents, SAC, SAMC and alliin,
prevented the generation of membrane damaging free radicals (7). Their results
support previous research showing that AGE and SAC protect vascular endothelial
cells from hydrogen-peroxide induced oxidant injury (8). Since SAC is well
absorbed, these studies suggest that SAC and AGE may be useful as free radical
scavengers of compounds such as hydrogen peroxide and its resultant peroxyl
radical in the body. AGE
and its various constituents also prevented damage to cells induced by oxidized
LDL. Oxidation of LDL cholesterol has been recognized as an important causative
factor in the progression of atherosclerosis.
LDL, the "bad" cholesterol carrying protein, delivers
cholesterol to the tissues (HDL, on the contrary, takes cholesterol away from
tissues). When LDL is oxidized, it
becomes "sticky" and is more likely to deposit cholesterol on the
lining of veins and arteries. Dr. Lau and his group from Loma Linda University
recently found that AGE and its various constituents could inhibit
copper-induced oxidation of LDL in a dose-dependant manner (9). Further, they
found that AGE and its various constituents, when incubated with cells, which
line the lungs, could prevent damage induced by oxidized LDL. References ![]()
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