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Free
Radicals, Antioxidants and SOD
Oxygen is necessary to sustain life, yet the very process of
oxygen metabolism in the cells creates destructive elements
called free radicals. Free radicals, or oxidants, are
chemically unbalanced, carrying free electrons that can
damage molecules in our cells while trying to achieve
balance – potentially damaging the cell itself. This free
radical damage, also called oxidative stress, is widely
accepted as the free radical theory of aging.
Fortunately, the body has its own free radical defense
system. Virtually every cell produces antioxidant enzymes
called Superoxide Dismutase (SOD), catalase and glutathione
peroxidase. 
These enzymes protect the cells during oxygen
metabolism, safely breaking down harmful free radicals to
balanced elements like H20.
Dietary antioxidants, such as the vitamins A, C, E, play a
secondary, supporting role. They act as free radical
scavengers by “donating” an electron to provide chemical
balance. These antioxidants become quickly saturated – only
once can they donate an electron.
Ideally,
the balance between the production of free radicals and our
antioxidant defenses is maintained.
However, our antioxidant defense system can become
overwhelmed. Studies indicate the levels of SOD, catalase
and Gpx decrease with age. Also, certain conditions are
related to the increased production of unstable oxygen
derivatives, including physical stress, health challenges
and exposure to environmental toxins such as smoking and
pollution.
When the
antioxidant systems of defense are overloaded, oxidative
stress (free radicals in excess) may occur.
For
this reason, many antioxidant products, including
supplements and functional foods, are being developed.
However, the bioactivity of dietary antioxidants is often
quite low, and the amounts needed to be consumed daily to
combat free radicals and inhibit oxidative stress are
prohibitive. In addition, this approach is designed to
correct a possible antioxidant deficiency, and does not
specifically promote the body’s own endogenous antioxidant
defenses.
GliSODin is
the first orally available delivery of SOD
The
benefits of SOD, catalase and glutathione peroxidase are
well established and seemingly a supplement would be
beneficial. However, these are protein enzymes and they are
broken down by stomach acids and the digestive process.
(Any living thing that metabolizes oxygen, including fruits
and vegetables, produces SOD, thus we consume it every day –
but it is destroyed during digestion, providing no
benefits.) Bovine SOD, which is offered by some marketers,
has the same problem.
GliSODin's patented combination of a melon-derived SOD
protected by a wheat gliadin layer is designed to protect
fragile SOD from degradation during digestion. Gliadin is
also bio-adhesive, and in particular adheres to the wall of
the small intestine. It progressively releases the SOD and
eases its passage through the intestinal mucosa towards the
blood circulation ensuring the SOD’s delivery and
bioactivity.
GliSODin
specifically acts as a catalyst, promoting the body’s own
antioxidant defenses, including SOD, catalase, and
glutathione peroxidase. This process results in specific
therapeutic benefits.
Scientifically Validated Efficacy
Initial laboratory studies have been published, providing
important proof-of-concept evidence of efficacy. GliSODin
supplementation was shown to promote circulating levels SOD,
Catalase and glutathione peroxidase (Gpx) in animal models.
Further studies shown increases in these antioxidant defense
enzymes in several important organs. Finally, extensive
safety studies were undertaken.
Human
Research
Human studies have demonstrated GliSODin’s ability to
promote the production of the body’s endogenous
antioxidants, including SOD. In one such study, an
unpublished, randomized, double blind, placebo-controlled
clinical trial conducted in the Ivory Coast, test subjects
with reduced levels of SOD, Catalase and Gpx received either
melon-sourced SOD (n=12), GliSODin; n=11) or placebo (n=12)
for 21 days. A significant restoration of circulating
antioxidant levels was observed in the GliSODin group,
whereas no change was observed in participants given
unprotected melon-sourced SOD or placebo. The researchers
concluded only the GliSODin preparation was able to
efficiently support the antioxidant defenses.
Protection
of cellular
DNA against
oxidative stress
Beyond demonstrating GliSODin's bioavailability, several
clinical trials back the ability of the compound to prevent
oxidative damage. In a double-blind study published in 2004
showed administration of GliSODin protected DNA from
oxidative damage in subjects exposed to accelerated
oxidative stress using a hyperbaric chamber.
Subjects
given GliSODin had fewer
DNA strand breaks and lower serum levels of isoprostane than
subjects given placebo. This was particularly important as
GliSODin was the first antioxidant to demonstate this
protective benefit. In this model, oral antioxidants such
as Vitamin E or N-acetylcysteine did not provide
DNA
protection.
Inhibition
of UV oxidative stress
GliSODin was also shown to inhibit oxidative damage in a
proprietary trial involving skin burn induced by UV
radiation. In the double blind, placebo-controlled study,
conducted at Center Hospital University and presented at the
2005 meeting of the Annual Congress of Dermatological
Research (CARD) in Brest, France, ultra-violet (UV) skin
burn was induced on the inner forearms of healthy subjects
who were then randomized to receive GliSODin or placebo for
four weeks.
Skin
color was measured by chromometry, and changes in skin
inflammation were assessed by monitoring congestion of small
blood vessels. SOD supplementation resulted in an increase
in the minimum exposure to UV rays necessary to produce skin
burn. In particular, fair-skinned test subjects given
GliSODin required eight times greater exposure to UV rays to
contract skin burn after 30 days’ supplementation compared
to baseline. This benefit was not found in individuals
administered placebo.
GliSODin
was also shown to inhibit oxidative damage to skin in
another proprietary, open, 60-day trial conducted 150
volunteers divided into three groups and given 500 mg/d of
GliSODin 15 days prior to and during sun exposure.
Group 1 included 75 patients prone to flushing, Group 2
consisted of 60 patients with sun allergy and Group 3
contained 15 patients susceptible to other sun-related
reactions including pruritus, solar eczema and rashes. The
test subjects sunbathed as usual and continued to use their
regular sun screen (sun protection factor [SPF] 20 to 100).
In Group 1, 85 percent had no sunburn, 8 percent had
diminished episodes and 6 percent contracted sunburn. In
Group 2, 73 percent of test subjects did not experience
allergic reaction, 10 percent had a reduced reaction and 16
percent sustained an allergic reaction. All patients in
Group 3 showed no negative reactions; overall, 86 percent of
test subjects showed no harmful sunlight-induced reactions.
Inhibition
of oxidative stress in the arteries
GliSODin was recently shown in a three-year study to
significantly protect vascular health in high-risk
individuals who would be considered to have Metabolic
Syndrome, or Syndrome X. In this trial the patients
followed the Lyon Heart Diet and made behavioral changes.
However, while the diet and lifestyle changes reduced the
risk factors, several measurements of oxidative stress and
the thickness of plaques in the carotid arteries were not
reduced. The addition of GliSODin significantly
reduced oxidative stress and within 9 months positively
impacted vascular health, showing a significant reduction in
plaques by the end of 24 months.
Several
new clinical trials involving GliSODin are currently in
progress. These include a study linking GliSODin
supplementation to positive cardiovascular benefits, and another trial examining GliSODin's ability to
inhibit UV stress in fair-skinned individuals. A human trial
examining the effect of GliSODin on eye health in the
elderly is scheduled for completion in 2008.
I,
Vouldoukis, M. Conti, P. Krauss, C. Kamate, S. Blazquez, M.
Tefit, D. Mazier, A. Calenda, B. Dugas. “Supplementation
with gliadin-combined plant superoxide dismutase extracts
promotes antioxidant defenses and protects against oxidative
stress,” Phytotherapy Res Mar 1;18(12) (2004) 957-96
H. Chenal,
A. Davit-Spraul, J. Brevet, A. Legrand, J. Demouzon, C.
Cosson. B. Dugas, L. Montagnier, M. Conti. “Restored
antioxidant circulating capacities in AIDS west african
patients receiving an antioxidant nutraceutical Cucumis melo
extract rich in superoxide dismutase activity,” (Abstract to
be presented at XVI International AIDS Conference 8/06)
C. Muth, Y. Glenz, M. Klaus, P. Radermacher, Guenter Speit,
X. Leverve.
“Influence
of an orally effective SOD on hyperbaric, oxygen related
cell damage,” Free Radical Research 38:9 (2004) pp. 927-932
PMID: 15621710
M.
Mac-Mary, J. Sainthillier, P. Creidi, J.P. Series, F. Vix,
Ph. Humbert, "Evaluation of the Effect of GliSODin on the
Intensity of Actinic Erythema," presented at the CARD
(Annual Congress of Dermatological Research) meeting in Brest, France,
May 28th 2005
J Menvielle-Bourg,
“Superoxide Dismutase (SOD), a Powerful Antioxidant, is now
Available Orally” Phytotherapie (2005) Numero 3: 118-121
M. Cloarec, et. al. “GliSODin, a Vegetal SOD with Gliadin, as Preventative Agent VS. Atherosclerosis, as Confirmed with Carotid Ultrasound-B Imaging,”
European Annuals of Allergy & Clinical Immunology vol 39 no 2 2007
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