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LE Magazine August 2005
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Super Oxide Dismutase (SOD)

Boosting your body’s store of the enzyme SOD provides powerful protection against oxidative stress. By John Colman

Another Powerful SOD Booster: GliSODin®

Elevating serum and blood levels of endogenous antioxidants such as SOD and catalase is a safe, natural way to reduce inflammation and pain. Like SODzyme™, another recently developed natural product called GliSODin® raises serum and tissue levels of SOD. GliSODin® is derived from an extract of cantaloupe bred to produce more SOD than ordinary melons.33,34

In 1980, melon growers noticed that some varieties of cantaloupe had a shelf life of 15 days, or three to four times longer than the shelf life of the average fully ripened melon. Extensive research demonstrated that these non-rotting cantaloupes contained much higher levels of SOD and catalase than did standard melons. Years of additional research involving crushing, filtering, centrifuging, and freeze-drying extracts of the melons produced SOD in a concentrated granule form that, when bonded to wheat protein, made it highly absorbable in and bioavailable to the human body.33,34

GliSODin® is a natural, plant-derived SOD that has been bonded to a wheat protein called gliadin for better absorption. In fact, it has taken 40 years of research to make SOD orally bioavailable, since unbound SOD is broken down rapidly in the stomach into its separate amino acid components. Its high molecular weight of 25-40,000 units also makes it difficult or impossible to pass through cell membranes, even if directly injected into the bloodstream.33-35

Most of the early arthritis research with SOD was done with bovine SOD that was injected into the joints and bloodstreams of laboratory animals and humans. While the human studies produced some dramatic results, injecting SOD into arthritic joints posed a logistical challenge, especially since exogenously derived bovine SOD is rapidly broken down.35

Extensive Research on GliSODin®

Numerous scientific studies have examined the effects of GliSODin®. In one landmark study, 20 volunteers in a hyperbaric chamber breathed pure oxygen at 2.5 atmospheres of pressure for one hour. Hyperbaric oxygen treatment serves as an in-vivo model of oxidative stress in humans. Subjects exposed to oxygen in a high-pressure chamber typically demonstrate increased levels of free radicals and DNA damage in their white blood cells that cannot be prevented by oral antioxidants such as vitamin E or N-acetylcysteine.36

In this study, the group supplemented with GliSODin® capsules had less DNA damage than subjects who did not supplement. The scientists concluded that GliSODin® helped prevent breaks in DNA strands that are associated with exposure to high-pressure oxygen. The results also suggest GliSODin® is readily absorbed in the gastrointestinal tract and makes its way into the cells themselves, something that even injectible bovine SOD failed to do in previous studies.36

An emerging marker of oxidative stress in humans is isoprostanes, which are generated by the peroxidation of fatty acids in cell membranes or lipoproteins. Clinical data indicate that an increased level of isoprostane biosynthesis is correlated with certain disease states related to oxidative stress.37 Human subjects who supplemented with GliSODin® capsules demonstrated lower baseline levels of isoprostanes—of 14.0 picograms per milliliter (pg/ml)—compared to an average level of 16.8 pg/ml in a control group.36 After one hour in a hyperbaric oxygen chamber, isoprostane levels in the control group rose to 22.3 pg/ml, while the GliSODin®-supplemented group experienced no change in isoprostanes, demonstrating a sustained level of 14 pg/ml. Thus, GliSODin® appears to protect against cell membrane damage that occurs during normal oxygen exposure and in high-pressure oxygen environments. This study illustrates GliSODin®’s ability to limit daily oxidative damage from oxygen utilization, as well as to prevent the greater damage associated with conditions of severe oxidative stress.36

Another study found that small amounts of orally administered GliSODin® raised circulating blood levels of SOD by 89% in mice.33 Blood levels of catalase, another antioxidant enzyme, also increased to almost three times the level seen in a control group.33 Catalase is the enzyme that converts hydrogen peroxide to water, and high levels of hydrogen peroxide may contribute to inflammation and arthritis.34 The liver cells of the mice also demonstrated greatly increased levels of SOD and catalase, indicating that GliSODin® stimulates production of these critical antioxidants inside the major organs and deep tissues.33

The potent antioxidant properties of GliSODin® were also studied in mouse macrophages taken from live, normal mice. Macrophages are a type of immune responder cell that is activated in inflammatory processes such as arthritis. When treated with GliSODin®, macrophage cells produced fewer of the free radicals superoxide, nitrites, and peroxynitrite than did macrophages taken from untreated animals.34

Researchers studied the interaction of GliSODin® with inflammatory cytokines that play a role in arthritis. They found that untreated immune responder cells produced high levels of the inflammatory cytokine, tumor necrosis factor-alpha (TNF-a), and normal levels of an anti-inflammatory cytokine, interleukin-10 (IL-10). When treated with GliSODin®, however, the immune responder cells produced very low levels of inflammatory TNF-a in combination with very high levels of anti-inflammatory IL-10. Previous studies have suggested that people who live to 90 or 100 years of age have high blood levels of IL-10, which may keep their inflammatory reactions in check during aging. GliSODin® may thus promote a protective anti-inflammatory profile similar to that of people who live to extreme old age.34,38

Lactic acid is a metabolic by-product generated during strenuous exercise. In some forms of arthritis, the lactic acid content of joints is increased.39 Interventions that lower lactic acid levels in the blood and in joint fluids have been suggested to help modulate muscle and joint pain. Human studies demonstrated that four weeks of GliSODin® supplementation reduced lactic acid levels during strenuous cycling or treadmill exercise. The most strenuous exercise activity generated the highest levels of lactic acid. GliSODin® therapy exerted the most potent lactic acid-reducing effects in extreme cases of exercise-induced stress. GliSODin® may thus be indicated in reducing lactic acid levels related to exercise and certain pain-related conditions.40

A study of AIDS patients in Ivory Coast, Africa, found that GliSODin® supplementation minimized disease-related oxidative stress and helped restore immune cell function. Patients who received GliSODin® experienced a restoration of blood SOD levels and antioxidant status to values seen in uninfected controls. The AIDS patients demonstrated elevated levels of beta-2 microglobulin before taking GliSODin®, indicating an immune challenge. GliSODin® supplementation decreased beta-2 microglobulin levels, indicating a possible improvement in immune status that may correlate with strengthened antioxidant defense. Because these AIDS patients were not receiving anti-retroviral prescription therapy, their improvements were attributed to GliSODin®.41

GliSODin® GUARDS AGAINST SUNBURN

GliSODin® offers powerful protection against the effects of ultraviolet (UV) light, thus reducing susceptibility to sunburn, according to study results presented at the Annual Congress for Dermatological Research in Brest, France, in May 2005.*

Researchers at the Center Hospital University in Besançon, France, conducted a randomized, double-blind, placebo-controlled study of the effects of the SOD supplement GliSODin® in humans. The investigators used UV light to induce sunburn on the forearms of 50 subjects once a week for four weeks. The participants took a supplement containing either GliSODin® or placebo each day, beginning two to three days before the first irradiation. The researchers used chromometry to measure skin color and videocapillaroscopy to measure inflammatory changes in the skin.
The GliSODin®-supplemented group experienced a significant increase in the minimum amount of exposure necessary to produce sunburn. Even fair-skinned people required eight times more UV exposure to produce sunburn than did the placebo group. Once burning occurred, the redness decreased more rapidly in the GliSODin® group than in the placebo group. The supplemented group also demonstrated less skin inflammation. GliSODin® was extremely fast-acting, with just two to three days of supplementation before the first irradiation producing a noticeable difference compared to the placebo group.

“This study confirms the efficacy of GliSODin® in the prevention of the consequences of oxidative stress resulting from exposure to the sun. This efficacy is of particular interest for [fair-skinned individuals] that represent a major part of the consultations in dermatology,” said the researchers.
Previous human and laboratory studies have demonstrated GliSODin®’s effectiveness in protecting cells from oxidative stress by spurring the body’s production of endogenous antioxidants, including SOD, catalase, and glutathione peroxidase. These antioxidant enzymes are key elements of the “internal antioxidant defense system” that is so critical to countering free radicals produced by oxidative stress.

*Available at: http://www.npicenter.com/anm/templates/newsATemp.aspx?articleid=12601&zoneid=24. Accessed June 5, 2005.

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