GliSODin Backgrounder

 

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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